The gut microbiota undergoes continuous variations among individuals and across their lifespan, shaped by diverse factors encompassing diet, age, lifestyle choices, medication intake, and disease states. These microbial inhabitants play a pivotal role in orchestrating physiological metabolic pathways through the production of metabolites like bile acids, choline, short-chain fatty acids, and neurotransmitters, thereby establishing a dynamic "gut-organ axis" with the host. The intricate interplay between the gut microbiota and the host is indispensable for gut health, and RNA N6-methyladenosine modification, a pivotal epigenetic mark on RNA, emerges as a key player in this process. M6A modification, the most prevalent internal modification of eukaryotic RNA, has garnered significant attention in the realm of RNA epigenetics. Recent findings underscore its potential to influence gut microbiota diversity and intestinal barrier function by modulating host gene expression patterns. Conversely, the gut microbiota, through its impact on the epigenetic landscape of host cells, may indirectly regulate the recruitment and activity of RNA m6A-modifying enzymes. This review endeavors to delve into the biological functions of m6A modification and its consequences on intestinal injury and disease pathogenesis, elucidating the partial possible mechanisms by which the gut microbiota and its metabolites maintain host intestinal health and homeostasis. Furthermore, it also explores the intricate crosstalk between them in intestinal injury, offering a novel perspective that deepens our understanding of the mechanisms underlying intestinal diseases.

The human microbiome, a complex ecosystem of microbial communities, plays a crucial role in physiological processes, and emerging research indicates a potential link between it and reproductive cancers. This connection highlights the significance of understanding the microbiome's influence on cancer development and treatment. A comprehensive review of current literature was conducted, focusing on studies that investigate the relationship between microbiome composition, reproductive cancer progression, and potential therapeutic approaches to modulate the microbiome. Evidence suggests that imbalances in the microbiome, known as dysbiosis, may contribute to the development and progression of reproductive cancers. Specific microbial populations have been associated with inflammatory responses, immune modulation, and even resistance to conventional therapies. Interventions such as probiotics, dietary modifications, and fecal microbiota transplantation have shown promise in restoring healthy microbiome function and improving cancer outcomes in pre-clinical models, with pilot studies in humans indicating potential benefits. This review explores the therapeutic potential of microbiome modulation in the management of reproductive cancers, discussing the mechanisms involved and the evidence supporting microbiome-targeted therapies. Future research is warranted to unravel the complex interactions between the microbiome and reproductive cancer pathophysiology, paving the way for innovative approaches.

Colorectal carcinogenesis induces changes in the colon, such as the appearance of aberrant crypt foci (ACF). This process is influenced by genetic and environmental factors, such as diet. Hibiscus sabdariffa L. is a considerable source of phenolic compounds, such as anthocyanins, and dietary fibers that may exert anti-inflammatory, antioxidant and prebiotic properties, attenuating the appearance of ACFs.

To investigate whether supplementation with 5% or 10% of dehydrated calyces of Hibiscus sabadariffa (DHSC) influences the composition of the intestinal microbiota and the expression of genes related to colorectal carcinogenesis in BALB/c mice.

The in vivo experiment lasted 12 weeks and the animals were divided into 3 experimental groups: the control group and the supplemented groups (5% or 10% DCHS) and induced pre-neoplastic lesions with the drug Dimethylhydrazine. Serum aspartate aminotransferase and alanine aminotransferase markers, liver cytokine profile, gut microbiota composition and tumor protein 53, cellular myelocytomatosis oncogene, caspase-3 and Proliferating Cell Nuclear Antigen gene expression were determined.

Supplementation with 5% or 10% of DCHS altered the composition of the intestinal microbiota, increasing the abundance of the families Lachnospiraceae, Ruminococcaceae, Clostridiaceae and of the genus Clostridum, important producers of butyrate. Furthermore, 5% and 10% DCHS supplementation increased caspase-3 and c-Myc expression, respectively, which may suggest apoptotic events.

Therefore, the effects of DHSC, rich in anthocyanins and dietary fiber, on the composition of the intestinal microbiota and on the expression of genes associated with cell apoptosis may contribute to reducing the risk of developing preneoplastic lesions.

Gut microbiota is associated with endometrial cancer (EC); however, the causal relationship remains unexplored. This study attempted to explore the relationship between gut microbiota and EC using Mendelian randomization (MR) methods.

In this two-sample MR analysis, we used MiBioGen's gut microbiota data as the exposure and three datasets from European populations with EC as the outcome. The EC datasets included general EC, endometrioid histology, and non-endometrioid histology. Single nucleotide polymorphism (SNP) was used as the instrumental variable. Inverse variance weighted (IVW), multiplicative random effects IVW (MRE-IVW), Maximum likelihood (ML), MR Egger, MR-PRESSO, and the weighted median were used to perform MR analysis. Sensitivity analysis was conducted to assess the reliability of the results.

In this MR analysis of three EC datasets, specific gut microbiota were identified as potentially associated with different pathological types of EC. For general EC (ID: ebi-a-GCST006464), Family.Acidaminococcaceae (OR = 1.23, 95%CI: 1.02-1.48) and genus.Butyrivibrio (OR = 1.08, 95%CI: 1.01-1.16) were identified as risk factors, while genus.Ruminococcaceae UCG014 (OR = 0.82, 95%CI: 0.69-0.98) and genus.Turicibacter (OR = 0.84, 95%CI: 0.73-0.97) appeared to have protective effects. For endometrioid histology EC (ID: ebi-a-GCST006465), Family.Acidaminococcaceae (OR = 1.27, 95%CI: 1.01-1.59) and genus.Butyrivibrio (OR = 1.10, 95%CI: 1.01-1.19) were identified as risk factors, while several microbiota, including Family.Lactobacillaceae, genus.Coprococcus3, genus.Dorea, genus.Flavonifractor, genus.Lactobacillus, genus.Paraprevotella, and genus.Turicibacter, were identified as protective factors. For non-endometrioid histology EC (ID: ebi-a-GCST006466), Family.Rhodospirillaceae (OR = 1.41, 95%CI: 1.01-1.96) and genus.Peptococcus (OR = 1.43, 95%CI: 1.07-1.91) were identified as risk factors, while no significant protective factors were identified.

This two-sample MR study has identified gut microbiota with potential causal relationships with EC, varying by pathological type. These findings provide new insights into the pathogenesis of EC and suggest directions for future research on diagnosis and treatment strategies.

Inflammatory bowel diseases (IBD) including Crohn's disease (CD) and ulcerative colitis (UC) are chronic, relapsing conditions characterized by dysregulated immune responses and persistent intestinal inflammation. This review aims to examine new potential therapeutic targets in IBD starting from the STRIDE-II statements. Key targets now include clinical remission, endoscopic remission, and biomarker normalization (such as C-reactive protein and fecal calprotectin). Moreover, histologic remission, transmural remission, and in the future molecular targets are emerging as important indicators of sustained disease control. The treatment goals for inflammatory bowel disease are varied: to relieve symptoms, prevent permanent intestinal damage, promote inflammation remission, and minimize complications. Consequently, the therapeutic targets have evolved to become broader and more ambitious. Integrating these advanced therapeutic targets has the potential to redefine IBD management by promoting deeper disease control and improved patient outcomes. Further research is essential to validate these strategies and optimize their clinical implementation.

Globally, one of the most prevalent cancers is colorectal cancer (CRC). Chemotherapy and surgery are two common conventional CRC therapies that are frequently ineffective and have serious adverse effects. Thus, there is a need for complementary and different therapeutic approaches. The use of microbial metabolites to trigger epigenetic alterations as a way of preventing CRC is one newly emerging field of inquiry. Small chemicals called microbial metabolites, which are made by microbes and capable of altering host cell behaviour, are created. Recent research has demonstrated that these metabolites can lead to epigenetic modifications such as histone modifications, DNA methylation, and non-coding RNA regulation, which can control gene expression and affect cellular behaviour. This review highlights the current knowledge on the epigenetic modification for cancer treatment, immunomodulatory and anti-carcinogenic attributes of microbial metabolites, gut epigenetic targeting system, and the role of dietary fibre and gut microbiota in cancer treatment. It also focuses on short-chain fatty acids, especially butyrates (which are generated by microbes), and their cancer treatment perspective, challenges, and limitations, as well as state-of-the-art research on microbial metabolites-induced epigenetic changes for CRC inhibition. In conclusion, the present work highlights the potential of microbial metabolites-induced epigenetic modifications as a novel therapeutic strategy for CRC suppression and guides future research directions in this dynamic field.

Background and Objectives: Radon is a known risk factor for lung cancer, and residential radon exposure is the leading cause of lung cancer in never smokers; however, in Italy, there is still a lack of public awareness regarding the risk caused by residential radon exposure. In this mortality study, which was carried out in an Italian Apulian town (Locorotondo) of the Bari province, we aimed to analyze lung cancer mortality and all-cause mortality in a population highly exposed to radon. Materials and Methods: The study period was 1998-2021. Local and Italian population and national mortality data were collected from the Italian National Institute of Statistics (ISTAT) website platform. Local mortality data were collected using copies of the Local Health Authority death certificates. Results: We identified 117 lung cancers in the studied period. The mortality data trends revealed a decrease in the all-causes standardized mortality ratios (SMRs), increases in the incidence rates of lung cancer and colorectal cancer in recent years, and a decrease in the incidence of noncancer diseases. We also found high SMRs for colorectal cancer until 2016 among older females. With respect to the cardio-circulatory system, only in 2014 did the male SMRs significantly influence the total SMR; after this period, a decreasing stable trend was observed. Conclusions: The natural balance of the population is decreasing, and mortality is decreasing for all causes. A future study will be needed to assess the associations between observed lung cancer cases and domestic radon exposure to drive radon mitigation and public health strategies.

Introduction: Nutritional metabolomics provides a comprehensive overview of the biochemical processes that are induced by dietary intake through the measurement of metabolite profiles in biological samples. However, there is a lack of deep phenotypic analysis that shows how dietary interventions influence the metabolic state across multiple physiologic sites. Dietary amino acids have emerged as important nutrients for physiology and pathophysiology given their ability to impact cell metabolism. Methods: The aim of the current study is to evaluate the effect of modulating amino acids in diet on the metabolome and microbiome of mice. Here, we report a comprehensive metabolite profiling across serum, liver, and feces, in addition to gut microbial analyses, following a reduction in either total dietary protein or diet-derived non-essential amino acids in mice. Results: We observed both distinct and overlapping patterns in the metabolic profile changes across the three sample types, with the strongest signals observed in liver and serum. Although amino acids and related molecules were the most commonly and strongly altered group of metabolites, additional small molecule changes included those related to glycolysis and the tricarboxylic acid cycle. Microbial profiling of feces showed significant differences in the abundance of select species across groups of mice. Conclusions: Our results demonstrate how changes in dietary amino acids influence the metabolic profiles across organ systems and the utility of metabolomic profiling for assessing diet-induced alterations in metabolism.

Colorectal cancer (CRC) is a major global health concern, with rising incidence and mortality rates. Conventional treatments often come with significant complications, prompting the exploration of natural compounds like curcumin as potential therapeutic agents. Using bioinformatic tools, this study investigated the role of curcumin in CRC treatment. Significant protein interactions between curcumin and target proteins were identified in the STITCH database. Differentially expressed genes (DEGs) associated with CRC were then analyzed from GEO databases. Comparing curcumin targets and CRC-related DEGs, nine significant common targets were identified: DNMT1, PCNA, CCND1, PLAU, MMP3, SOX9, FOXM1, CXCL2, and SERPINB5. Pathway enrichment analyses revealed that curcumin-targeted pathways were primarily related to p53, IL-17, NF-kappa B, TNF, and cell cycle signaling, all crucial in CRC development and progression. Further analyses using DAID and EnrichR algorithms showed that the curcumin targets exhibited greater specificity to bronchial epithelial cells and colorectal adenocarcinoma than other diseases. Analyses via the DSigDB database indicated that curcumin ranks highly among other drugs targeting the identified CRC-related genes. Docking studies revealed favorable binding interactions between curcumin and the key CRC-related proteins, suggesting potential molecular mechanisms by which curcumin may exert its effects. In summary, this study provides bioinformatic and docking evidence that curcumin may exert beneficial effects on CRC by modulating the expression or activity of multiple CRC-susceptibility genes involved in critical signaling pathways. These findings warrant further experimental validation and support the potential of curcumin as a therapeutic agent for CRC.

Globally, colorectal cancer (CRC) is a leading cause of cancer-related mortality. Dietary habits, inflammation, hereditary characteristics, and gut microbiota are some of its causes. The gut microbiota, a diverse population of bacteria living in the digestive system, has an impact on a variety of parameters, including inflammation, DNA damage, and immune response. The gut microbiome has a significant role in colon cancer susceptibility. Many studies have highlighted dysbiosis, an imbalance in the gut microbiota's makeup, as a major factor in colon cancer susceptibility. Dysbiosis has the potential to produce toxic metabolites and pro-inflammatory substances, which can hasten the growth of tumours. The ability of the gut microbiota to affect the host's immune system can also influence whether cancer develops or not. By better comprehending these complex interactions between colon cancer predisposition and gut flora, new preventive and therapeutic techniques might be developed. Targeting the gut microbiome with dietary modifications, probiotics, or faecal microbiota transplantation may offer cutting-edge approaches to reducing the risk of colon cancer and improving patient outcomes. The complex connection between the makeup of the gut microbiota and the emergence of colorectal cancer is explored in this narrative review.

Colorectal cancer (CRC) is the third most common cancer worldwide and the second leading cause of cancer-related death. Over the past two decades, numerous researchers have provided important evidence regarding the role of tight junction (TJ) proteins in the occurrence and progression of CRC. The causal relationship between the presence of specific TJ proteins and the development of CRC has also been confirmed. Despite the large number of publications in this field, a bibliometric study to review the current state of research and highlight the research trends and hotspots in this field has not yet been performed.

To analyze research on TJs and CRC, summarize the field's history and current status, and predict future research directions.

We searched the Science Citation Index Expanded database for all literature on CRC and TJs from 2001-2023. We used bibliometrics to analyze the data of these papers, such as the authors, countries, institutions, and references. Co-authorship, co-citation, and co-occurrence analyses were the main methods of analysis. CiteSpace and VOSviewer were used to visualize the results.

A total of 205 studies were ultimately identified. The number of publications on this topic has steadily increased since 2007. China and the United States have made the largest contributions to this field. Anticancer Research was the most prolific journal, publishing 8 articles, while the journal Oncogene had the highest average citation rate (68.33). Professor Dhawan P was the most prolific and cited author in this field. Co-occurrence analysis of keywords revealed that "tight junction protein expression", "colorectal cancer", "intestinal microbiota", and "inflammatory bowel disease" had the highest frequency of occurrence, revealing the research hotspots and trends in this field.

This bibliometric analysis evaluated the scope and trends of TJ proteins in CRC, providing valuable research perspectives and future directions for studying the connection between the two. It is recommended to focus on emerging research hotspots, such as the correlations among intestinal microbiota, inflammatory bowel disease, TJ protein expression, and CRC.

The purpose of this study was to demonstrate the regulatory effect of berberine (BBR) on the intestinal microbiota and related epigenetics during the inhibition of colon cancer cell growth in vitro and in vivo. We used a nude mouse xenograft model with HT29 colon cancer cells to establish and divide into a model group and BBR group. The mice were treated for four weeks, and HT29 cells in the BBR group were cultured for 48 h. Cetuximab and the DNA transmethylase (DNMT) inhibitor 5-AZA-dC were added to HT29 cells. Tumour volume and weight were measured by hematoxylin-eosin (HE) staining for histopathological observation. Mouse faeces were collected, and the gut microbiota was analysed with 16S rDNA amplicons. The levels of cytokines in the supernatant of HT29 cells were measured by ELISA. A CCK-8 kit was used to examine the proliferation of HT29 cells, and RT‒PCR was used to measure the levels of c-Myc, DNMT1, DNMT3A, and DNMT3B. We found that BBR reduced the growth of colon cancer cells to a certain extent in vitro and in vivo, although the difference was not statistically significant compared with that in the model group. BBR significantly mediated the abundance, composition and metabolic functions of the intestinal microbial flora in mice with colon cancer. The effect of BBR on inflammatory cytokines, including IL-6, FGF, and PDGF, was not obvious, but BBR significantly downregulated IL-10 levels (P < 0.05) and reduced c-Myc, DNMT1, and DNMT3B levels (P < 0.05). Inhibiting DNMTs with 5-AZA-dC significantly suppressed the proliferation of HT29 cells, which was consistent with the effect of BBR. The inhibitory effect of berberine on colon cancer is related not only to the intestinal microbiota and its metabolic functions but also to the regulation of DNMTs.

Inflammatory bowel diseases (IBD) remain challenging in terms of understanding their causes and in terms of diagnosing, treating, and monitoring patients. Modern diagnosis combines biomarkers, imaging, and endoscopic methods. Common biomarkers like CRP and fecal calprotectin, while invaluable tools, have limitations and are not entirely specific to IBD. The limitations of existing markers and the invasiveness of endoscopic procedures highlight the need to discover and implement new markers. With an ideal biomarker, we could predict the risk of disease development, as well as the possibility of response to a particular therapy, which would be significant in elucidating the pathogenesis of the disease. Recent research in the fields of machine learning, proteomics, epigenetics, and gut microbiota provides further insight into the pathogenesis of the disease and is also revealing new biomarkers. New markers, such as BAFF, PGE-MUM, oncostatin M, microRNA panels, αvβ6 antibody, and S100A12 from stool, are increasingly being identified, with αvβ6 antibody and oncostatin M being potentially close to being presented into clinical practice. However, the specificity of certain markers still remains problematic. Furthermore, the use of expensive and less accessible technology for detecting new markers, such as microRNAs, represents a limitation for widespread use in clinical practice. Nevertheless, the need for non-invasive, comprehensive markers is becoming increasingly important regarding the complexity of treatment and overall management of IBD.

The research on the correlation or causality between gut microbiota and the occurrence, development, and treatment of colorectal cancer (CRC) is receiving increasing emphasis. At the same time, the incidence and mortality of colorectal cancer vary among individuals and regions, as does the gut microbiota. In order to gain a better understanding of the characteristics of the gut microbiota in CRC patients and the differences between different regions, we initially compared the gut microbiota of 25 CRC patients and 26 healthy controls in the central region of China (Hubei Province) using 16S rRNA high-throughput sequencing technology. The results showed that Corynebacterium, Enterococcus, Lactobacillus, and Escherichia-Shigella were significantly enriched in CRC patients. In addition, we also compared the potential differences in functional pathways between the CRC group and the healthy control group using PICRUSt's functional prediction analysis. We then analyzed and compared it with five cohort studies from various regions of China, including Central, East, and Northeast China. We found that geographical factors may affect the composition of intestinal microbiota in CRC patients. The composition of intestinal microbiota is crucial information that influences colorectal cancer screening, early detection, and the prediction of CRC treatment outcomes. This emphasizes the importance of conducting research on CRC-related gut microbiota in various regions of China.

Colorectal cancer is the second deadliest cancer in the world, and its prevalence has been increasing alarmingly in recent years. After researchers discovered the existence of dysbiosis in colorectal cancer, they considered the use of probiotics in the treatment of colorectal cancer. However, for various reasons, including the low safety profile of probiotics in susceptible and immunocompromised patient5s, and the risk of developing antibiotic resistance, researchers have shifted their focus to non-living cells, their components, and metabolites. This review aims to comprehensively evaluate the literature on the effects of diet, microbiota, and postbiotics on colorectal cancer and the future of postbiotics.

The link between diet, gut microbiota, and colorectal cancer has been established primarily as a relationship rather than a cause-effect relationship. The gut microbiota can convert gastrointestinal tract and dietary factors into either onco-metabolites or tumor suppressor metabolites. There is serious dysbiosis in the microbiota in colorectal cancer. Postbiotics appear to be promising agents in the prevention and treatment of colorectal cancer. It has been shown that various postbiotics can selectively induce apoptosis in CRC, inhibit cell proliferation, growth, invasion, and migration, modulate the immune system, suppress carcinogenic signaling pathways, maintain intestinal epithelial integrity, and have a synergistic effect with chemotherapy drugs. However, it is also reported that some postbiotics are ineffective and may be risky in terms of safety profile in some patients. Many issues need to be researched about postbiotics. Large-scale, randomized, double-blind clinical studies are needed.

Gut microbiota interacts with host epithelial cells and regulates many physiological functions such as genetics, epigenetics, metabolism of nutrients, and immune functions. Dietary factors may also be involved in the etiology of colorectal cancer (CRC), especially when an unhealthy diet is consumed with excess calorie intake and bad practices like smoking or consuming a great deal of alcohol. Bacteria including Fusobacterium nucleatum, Enterotoxigenic Bacteroides fragilis (ETBF), and Escherichia coli (E. coli) actively participate in the carcinogenesis of CRC. Gastrointestinal tract with chronic inflammation and immunocompromised patients are at high risk for CRC progression. Further, the gut microbiota is also involved in Geno-toxicity by producing toxins like colibactin and cytolethal distending toxin (CDT) which cause damage to double-stranded DNA. Specific microRNAs can act as either tumor suppressors or oncogenes depending on the cellular environment in which they are expressed. The current review mainly highlights the role of gut microbiota in CRC, the mechanisms of several factors in carcinogenesis, and the role of particular microbes in colorectal neoplasia.

Processed meat, as an important part of the human diet, has been recognized as a carcinogen by the International Agency for Research on Cancer (IARC). Although numerous epidemiological reports supported the IARC's view, the relevant evidence of a direct association between processed meat and carcinogenicity has been insufficient and the mechanism has been unclear. This study aims to investigate the effects of pork sausage (as a representative example of processed meat) intake on gut microbial communities and metabolites of mice. Microbial communities and metabolites from all groups were analyzed using 16S rRNA gene sequencing and Ultra performance liquid chromatography-quadrupole-time of flight-mass spectrometer (UPLC-Q-TOF/MS), respectively.

The levels of Bacteroidetes, Bacteroides, Alloprevotella, Lactobacillus, Prevotella_9, Lachnospiraceae_NK4A136_group, Alistipes, Blautia, Proteobacteria, Firmicutes, Allobaculum, Helicobacter, Desulfovibrio, Clostridium_sensu_stricto_1, Ruminococcaceae_UCG-014, Lachnospiraceae_UCG-006 and Streptococcus (P < 0.05) were obviously altered in the mice fed a pork sausage diet. Twenty-seven metabolites from intestinal content samples and fourteen matabolites from whole blood samples were identified as potential biomarkers from multivariate analysis, including Phosphatidic acid (PA), Sphingomyelin (SM), Lysophosphatidylcholine (LysoPC), Diglyceride (DG), D-maltose, N-acylamides and so forth. The significant changes in these biomarkers demonstrate metabonomic variations in pork sausage treated rats, especially carbohydrate metabolism, lipid metabolism, and amino acid metabolism.

The present study provided evidence that a processed meat diet can increase the risk of colorectal cancer and other diseases significantly by altering the microbial community structure and disrupting the body's metabolic pathways. © 2023 Society of Chemical Industry.

Nonalcoholic fatty liver disease (NAFLD) is a stress-induced liver injury related to heredity, environmental exposure and the gut microbiome metabolism. Short-chain fatty acids (SCFAs), the metabolites of gut microbiota (GM), participate in the regulation of hepatic steatosis and inflammation through the gut-liver axis, which play an important role in the alleviation of NAFLD. However, little progress has been made in systematically elucidating the mechanism of how SCFAs improve NAFLD, especially the epigenetic mechanisms and the potential therapeutic application as clinical treatment for NAFLD. Herein, we adopted PubMed and Medline to search relevant keywords such as 'SCFAs', 'NAFLD', 'gut microbiota', 'Epigenetic', 'diet', and 'prebiotic effect' to review the latest research on SCFAs in NAFLD up to November 2023. In this review, firstly, we specifically discussed the production and function of SCFAs, as well as their crosstalk coordination in the gut liver axis. Secondly, we provided an updated summary and intensive discussion of how SCFAs affect hepatic steatosis to alleviate NAFLD from the perspective of genetic and epigenetic. Thirdly, we paid attention to the pharmacological and physiological characteristics of SCFAs, and proposed a promising future direction to adopt SCFAs alone or in combination with prebiotics and related clinical drugs to prevent and treat NAFLD. Together, this review aimed to elucidate the function of SCFAs and provide new insights to the prospects of SCFAs as a therapeutic target for NAFLD.

Earlier evidence that targeting the balance between histone acetyltransferases (HATs) and deacetylases (HDACs), through exposure to HDAC inhibitors (HDACis), could enhance skeletal myogenesis, prompted interest in using HDACis to promote muscle regeneration. Further identification of constitutive HDAC activation in dystrophin-deficient muscles, caused by dysregulated nitric oxide (NO) signaling, provided the rationale for HDACi-based therapeutic interventions for Duchenne muscular dystrophy (DMD). In this review, we describe the molecular, preclinical, and clinical evidence supporting the efficacy of HDACis in countering disease progression by targeting pathogenic networks of gene expression in multiple muscle-resident cell types of patients with DMD. Given that givinostat is paving the way for HDACi-based interventions in DMD, next-generation HDACis with optimized therapeutic profiles and efficacy could be also explored for synergistic combinations with other therapeutic strategies.

Colorectal cancer (CRC) is the second-highest cause of cancer-associated mortality among both men and women worldwide. One of the risk factors for CRC is obesity, which is correlated with a high-fat diet prevalent in Western dietary habits. The association between an obesogenic high-fat diet and CRC has been established for several decades; however, the mechanisms by which a high-fat diet increases the risk of CRC remain unclear. Recent studies indicate that gut microbiota strongly influence the pathogenesis of both high-fat diet-induced obesity and CRC. The gut microbiota is composed of hundreds of bacterial species, some of which are implicated in CRC. In particular, the expansion of facultative anaerobic Enterobacteriaceae, which is considered a microbial signature of intestinal microbiota functional imbalance (dysbiosis), is associated with both high-fat diet-induced obesity and CRC. Here, we review the interaction between the gut microbiome and its metabolic byproducts in the context of colorectal cancer (CRC) during high-fat diet-induced obesity. In addition, we will cover how a high-fat diet can drive the expansion of genotoxin-producing Escherichia coli by altering intestinal epithelial cell metabolism during gut inflammation conditions.

The association between dysbiotic microbiota biofilm and colon cancer has recently begun to attract attention. In the study, the apitherapeutic effects of bee products (honey, bee venom, royal jelly, pollen, perga and propolis) obtained from the endemic Yığılca ecotype of Apis mellifera anatoliaca were investigated. Antibiofilm activity were performed by microplate assay using crystal violet staining to measure adherent biofilm biomass of Escherichia coli capable of forming biofilms. Bee venom showed the highest inhibition effect (73.98%) at 50% concentration. Honey, perga and royal jelly reduced biofilm formation by >50% at all concentrations. The antiproliferation effect on the HCT116 colon cancer cell line was investigated with the water‑soluble tetrazolium salt‑1 assay. After 48 h of honey application at 50% concentration, cell proliferation decreased by 86.51%. The high cytotoxic effects of royal jelly and bee venom are also remarkable. Additionally, apoptotic pathway analysis was performed by ELISA using caspase 3, 8 and 9 enzyme-linked immunosorbent assay kits. All bee products induced a higher expression of caspase 9 compared with caspase 8. Natural products that upregulate caspase proteins are promising therapeutic targets for proliferative diseases.

Gastrointestinal (GI) cancers constitute more than 33% of new cancer cases worldwide and pose a considerable burden on public health. There exists a growing body of evidence that has systematically recorded an upward trajectory in GI malignancies within the last 5 to 10 years, thus presenting a formidable menace to the health of the human population. The perturbations in GI microbiota may have a noteworthy influence on the advancement of GI cancers; however, the precise mechanisms behind this association are still not comprehensively understood. Some bacteria have been observed to support cancer development, while others seem to provide a safeguard against it. Recent studies have indicated that alterations in the composition and abundance of microbiomes could be associated with the progression of various GI cancers, such as colorectal, gastric, hepatic, and esophageal cancers. Within this comprehensive analysis, we examine the significance of microbiomes, particularly those located in the intestines, in GI cancers. Furthermore, we explore the impact of microbiomes on various treatment modalities for GI cancer, including chemotherapy, immunotherapy, and radiotherapy. Additionally, we delve into the intricate mechanisms through which intestinal microbes influence the efficacy of GI cancer treatments.

The intestinal microbiota is a community of microorganisms inhabiting the human intestines, potentially influencing both physiological and pathophysiological processes in the human body. Existing evidence suggests that nutrients can influence the modulation of the gut microbiota. However, there is still limited evidence regarding the effects of vitamin and mineral supplementation on the human gut microbiota through epigenetic modification. It is plausible that maintaining an adequate dietary intake of vitamin D, iron, fibre, zinc and magnesium may have a beneficial effect on alleviating inflammation in the body, reducing oxidative stress, and improving the condition of the intestinal microbiota through various epigenetic mechanisms. Moreover, epigenetics involves alterations in the phenotype of a cell without changing its fundamental DNA sequence. It appears that the modulation of the microbiota by various nutrients may lead to epigenetic regulation. The correlations between microbiota and epigenetics are potentially interdependent. Therefore, the primary objective of this review is to identify the complex relationships between diet, gut microbiota, and epigenetic regulation. These interactions could play a crucial role in systemic health.

Colon cancer is a serious health problem across the globe with various dietary lifestyle modifications. It arises as an inflammation mediated crypts in the colon epithelial cells and undergoes uncontrolled cell division and proliferation. Bacterial enzymes contribute to a major outbreak in colon cancer development upon the release of toxic metabolites from the gut microflora. Pathogen associated molecular patterns and damage associated molecular patterns triggers the NLPR3 inflammasome pathways that releases pro-inflammatory cytokines to induce cancer of the colon. Contributing to this, specific chemokines and receptor complexes attribute to cellular proliferation and metastasis. Bacterial enzymes synergistically attack the colon mucosa and degenerate the cellular integrity causing lysosomal discharge. These factors further instigate the Tol like receptors (TLRs) and Nod like receptors (NLRs) to promote angiogenesis and supply nutrients for the cancer cells. Myrtenal, a monoterpene, is gaining more importance in recent times and it is being widely utilized against many diseases such as cancers, neurodegenerative diseases and diabetes. Based on the research data's, the reviews focus on the anticancer property of myrtenal by emphasizing its therapeutic properties which downregulate the inflammasome pathways and other signalling pathways. Combination therapy is gaining more importance as they can target every variant in the cellular stress condition. Clinical studies with compounds like myrtenal of the monoterpenes family is provided with positive results which might open an effective anticancer drug therapy. This review highlights myrtenal and its biological potency as a cost effective drug for prevention and treatment of colon cancer.

Even in present-day times, cancer is one of the most fatal diseases. People are overwhelmed by pricey chemotherapy, immunotherapy, and other costly cancer therapies in poor and middle-income countries. Cancer cells grow under anaerobic and hypoxic conditions. Pyruvate is the final product of the anaerobic glycolysis pathway, and many cancer cells utilize pyruvate for their growth and development. The anaerobic microbiome produces many anti-cancer substances that can act as anti-tumor agents and are both feasible and of low cost. There are different mechanisms of action of the anaerobic microbiome, such as the production of short-chain fatty acids (SCFAs), and competition for the anaerobic environment includes the metabolic product pyruvate to form lactic acid for energy.

In this review, we have summarized the role of the metabolic approach of the anaerobic human microbiome in cancer prevention and treatment by interfering with cancer metabolite pyruvate. SCFAs possess decisive outcomes in condoning almost all the hallmarks of cancer and helping the spread of cancer to other body parts. Studies have demonstrated the impact and significance of using SCFA, which results from anaerobic bacteria, as an anti-cancer agent. Anaerobic bacteria-based cancer therapy has become a promising approach to treat cancer using obligate and facultative anaerobic bacteria because of their ability to penetrate and increase in an acidic hypoxic environment.

This review attempts to provide the interconnection of cancer metabolism and anaerobic microbiome metabolism with a focus on pyruvate metabolism to understand and design unique anaerobic microbiota-based therapy for cancer patients.

Aging is a strong risk factor for colorectal cancer (CRC). It is well established that gut microbial dysbiosis can play a role in the etiology of CRC. Although the composition of the gut microbial community changes with age and is reported to become more pro-inflammatory, it is unclear whether such changes are also pro-tumorigenic for the colon. To address this gap, we conducted fecal microbiota transplants (FMT) from young (DY, ~6 wk) and old (DO, ~72 wk) donor mice into young (8 wk) recipient mice that were pre-treated with antibiotics. After initiating tumorigenesis with azoxymethane, recipients were maintained for 19 wk during which time they received monthly FMT boosters. Compared to recipients of young donors (RY), recipients of old donors (RO) had an approximately 3-fold higher prevalence of histologically confirmed colon tumors (15.8 vs 50%, Chi2 P = .03), approximately 2-fold higher proliferating colonocytes as well as significantly elevated colonic IL-6, IL-1β and Tnf-α. Transcriptomics analysis of the colonic mucosa revealed a striking upregulation of mitochondria-related genes in the RO mice, a finding corroborated by increased mitochondrial abundance. Amongst the differences in fecal microbiome observed between DY and DO mice, the genera Ruminoclostridium, Lachnoclostridium and Marvinbryantia were more abundant in DY mice while the genera Bacteroides and Akkermansia were more abundant in DO mice. Amongst recipients, Ruminoclostridium and Lachnoclostridium were higher in RY mice while Bacteroides was higher in RO mice. Differences in fecal microbiota were observed between young and old mice, some of which persisted upon transplant into recipient mice. Recipients of old donors displayed significantly higher colonic proliferation, inflammation and tumor abundance compared to recipients of young donors. These findings support an etiological role for altered gut microbial communities in the increased risk for CRC with increasing age and establishes that such risk can be transmitted between individuals.

"Inflammatory bowel disease" (IBD) is a chronic, relapsing inflammatory disease of the intestinal tract that typically begins at a young age and might transit to colorectal cancer (CRC). In this manuscript, we discussed the epigenetic and metabolic change to present a extensive view of IBDs transition to CRC. This study discusses the possible biomarkers for evaluating the condition of IBDs patients, especially before the transition to CRC.

We searched "PubMed" and "Google Scholar" using the keywords from 2000 to 2022.

In this manuscript, interesting titles associated with IBD and CRC are discussed to present a broad view regarding the epigenetic and metabolic reprogramming and the biomarkers.

Epigenetics can be the main reason in IBD transition to CRC, and Hypermethylation of several genes, such as VIM, OSM4, SEPT9, GATA4 and GATA5, NDRG4, BMP3, ITGA4 and plus hypomethylation of LINE1 can be used in IBD and CRC management. Epigenetic, metabolisms and microbiome-derived biomarkers, such as Linoleic acid and 12 hydroxy 8,10-octadecadienoic acid, Serum M2-pyruvate kinase and Six metabolic genes (NAT2, XDH, GPX3, AKR1C4, SPHK and ADCY5) expression are valuable biomarkers for early detection and transition to CRC condition. Some miRs, such as miR-31, miR-139-5p, miR -155, miR-17, miR-223, miR-370-3p, miR-31, miR -106a, miR -135b and miR-320 can be used as biomarkers to estimate IBD transition to CRC condition.

The complex mechanism of colorectal cancer development is closely associated with epigenetic modifications and is caused by overexpression and/or inactivation of oncogenes. Histone modifying enzymes catalyze histone modifications to alter gene expression, which plays a crucial role in the development and progression of colorectal cancer. Currently, there is more frequent study on histone acetylation, methylation, and phosphorylation, and their mechanisms in colorectal cancer development are clearer. This article elaborates on the role of histone modification in epigenetics in colorectal cancer development and discusses recent advances in using it as biomarkers and therapeutic targets for the treatment of colorectal cancer. The review aims to demonstrate the significant role of histone modification as a new therapeutic target in colorectal cancer and provides insights into the novel diagnostic and therapeutic options it offers.

Colorectal cancer (CRC) is a significant global health concern. Microbial dysbiosis and associated metabolites have been associated with CRC occurrence and progression. This study aims to analyze the gut microbiota composition and the enriched metabolic pathways in patients with late-stage CRC. In this study, a cohort of 25 CRC patients diagnosed at late stage III and IV and 25 healthy participants were enrolled. The fecal bacterial composition was investigated using V3-V4 ribosomal RNA gene sequencing, followed by clustering and linear discriminant analysis (LDA) effect size (LEfSe) analyses. A cluster of ortholog genes' (COG) functional annotations and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were employed to identify enrichment pathways between the two groups. The findings showed that the fecal microbiota between the two groups varied significantly in alpha and beta diversities. CRC patients' fecal samples had significantly enriched populations of Streptococcus salivarius, S. parasanguins, S. anginosus, Lactobacillus mucosae, L. gasseri, Peptostreptococcus, Eubacterium, Aerococcus, Family XIII_AD3001 Group, Erysipelatoclostridium, Escherichia-Shigella, Klebsiella, Enterobacter, Alistipes, Ralstonia, and Pseudomonas (Q < 0.05). The enriched pathways identified in the CRC group were amino acid transport, signaling and metabolism, membrane biogenesis, DNA replication and mismatch repair system, and protease activity (Q < 0.05). These results suggested that the imbalance between intestinal bacteria and the elevated level of the predicated functions and pathways may contribute to the development of advanced CRC tumors. Further research is warranted to elucidate the exact role of the gut microbiome in CRC and its potential implications for use in diagnostic, prevention, and treatment strategies.

Diet, lifestyle, and gut microbiota composition are key risk factors for the progression of colon cancer. Probiotics are living microorganisms that can offer health benefits to the parasitifer when ingested in competent quantities. Several in vivo, in vitro, and clinical studies have demonstrated that probiotics can prevent and mitigate the development of colon cancer. The anti-colon cancer mechanisms of probiotics include the suppression of cell proliferation and the promotion of cancer cell apoptosis, immunomodulation, the modulation of intestinal microorganisms and their metabolism, strengthening the intestinal barrier, and antioxidant effects. This article describes the pathogenesis of colon cancer and the available therapeutic options. In addition, this paper reviews the mechanisms by which probiotics mitigate colon cancer as well as the mitigating effects of probiotic components and metabolites on colon cancer.

In Latin America and the Caribbean a considerable proportion of the population have excess body weight, do not meet the recommendations of physical activity and healthy diet, and have suboptimal rates of breastfeeding. Excess body weight is associated with at least 15 cancer sites, physical activity protects against three cancers, with some evidence suggesting a protective effect for eight more cancer sites, and sedentary behavior probably increases the risk of five cancer sites. Fiber and wholegrains protect against colorectal cancer, high intake of fruits and vegetables could reduce the risk of aerodigestive cancers; processed and red meat increase the risk of colorectal cancer; and very hot beverages are associated with esophageal cancer. Moreover, sugar-sweetened beverages and ultra-processed foods are a convincing cause for excess body weight, increasing cancer risk through this pathway, with some emerging evidence suggesting also direct pathways. Breastfeeding protects against breast cancer, and could protect against ovarian cancer. Taking this evidence into account, the Latin America and the Caribbean Code Against Cancer recommends the general public to maintain a healthy body weight, be physically active and limit sedentary behavior, eat a healthy diet (eat plenty of vegetables, fruits, wholegrains and legumes; avoid sugar-sweetened beverages and processed meat; and limit ultra-processed foods, red meat and very hot beverages), and breastfeed. Moreover, the Latin America and the Caribbean Code Against Cancer also includes a set of public policy recommendations for cancer prevention to inform policy makers and civil society about the need of policies to shape healthy environments and create opportunities to facilitate the adoption of the recommendations directed to the public.

Colorectal cancer (CRC) is more prevalent among some racial and ethnic minority and low socioeconomic status populations. Although the gut microbiota is a risk factor for CRC and varies with race and ethnicity, its role in CRC disparities remains poorly understood.

We examined the feasibility of recruiting sociodemographically diverse CRC patients for a microbiome study involving a home stool collection. We also explored whether race and ethnicity were associated with gut microbiome composition. We recruited Black/African American, Hispanic/Latino, and non-Hispanic White patients who were receiving care for active CRC to complete a comprehensive dietary and lifestyle survey, self-collect a stool sample, and complete an exit interview. Gut microbial diversity and composition were analyzed using 16S rRNA gene sequencing.

30 individuals consented (of 35 who were eligible and contacted) with 5 (17%) Black/African American, 11 (37%) Hispanic/Latino, and 14 (46%) non-Hispanic White. A total of 22 (73%) completed the dietary and lifestyle survey; 18 (63%) returned a stool sample. Even after controlling for socioeconomic, dietary, or treatment-related covariates, microbiome composition was associated with race and ethnicity. Fusobacteriota (a phylum associated with the development and progression of CRC) was significantly higher in the Black/African American group compared to others, and microbial diversity was higher in samples from non-Hispanic White individuals compared to Hispanic/Latino individuals.

Our study shows that it is feasible to recruit and collect stool samples from diverse individuals with CRC and found significant associations in gut microbial structure with race and ethnicity.

Colon cancer onset is strongly associated with the differences in microbial taxa in the gastrointestinal tract. Although recent studies highlight the role of individual taxa, the effect of a complex gut microbiome (GM) on the metabolome and host transcriptome is still unknown. We used a multi-omics approach to determine how differences in the GM affect the susceptibility to adenoma development in a rat model of human colon cancer. Ultra-high performance liquid chromatography mass spectrometry of feces collected prior to observable disease onset identified putative metabolite profiles that likely predict future disease severity. Transcriptome analyses performed after disease onset from normal colonic epithelium and tumor tissues show a correlation between GM and host gene expression. Integrated pathway analyses of the metabolome and transcriptome based on putatively identified metabolic features indicate that bile acid biosynthesis is enriched in rats with high tumors along with increased fatty acid metabolism and mucin biosynthesis. Targeted pyrosequencing of the Pirc allele indicates that the GM alters the mechanism of adenoma development and may drive an epigenetic pathway of tumor suppressor silencing. This study reveals how untargeted metabolomics identifies signatures of susceptibility and integrated analyses uncover pathways of differential mechanisms of loss of tumor suppressor gene function and for potential prevention and therapeutic intervention. IMPORTANCE The association between the gut microbiome and colon cancer is significant but difficult to test in model systems. This study highlights the association of differences in the pathogen-free gut microbiome to changes in the host transcriptome and metabolome that correlate with colon adenoma initiation and development in a rat genetic model of early colon cancer. The utilization of a multi-omics approach integrating metabolomics and transcriptomics reveals differences in pathways including bile acid biosynthesis and fatty acid metabolism. The study also shows that differences in gut microbiomes significantly alter the mechanism of adenoma formation, shifting from genetic changes to epigenetic changes that initiate the early loss of tumor suppressor function. These findings enhance our understanding of the gut microbiome's role in colon cancer susceptibility, offer insights into potential biomarkers and therapeutic targets, and may pave the way for future prevention and intervention strategies.

The history of Lynch syndrome changed definitively in 2000, when a study published in Gastroenterology demonstrated a significant reduction in mortality among individuals with Lynch syndrome who undergo regular endoscopic surveillance. As a consequence of this clinical evidence, all scientific societies developed guidelines, which highlighted the role of colonoscopy in the management of Lynch syndrome, especially for individuals at high risk of colorectal cancer. Over the years, these guidelines were modified and updated. Specialized networks were developed in order to standardize endoscopic surveillance programs and evaluate all the clinical data retrieved by the results of colonoscopies performed for both the screening and the surveillance of individuals with Lynch syndrome. Recent data show that the impact of colonoscopy (with polypectomy) on the prevention of colorectal cancer in individuals with Lynch syndrome is less significant than previously thought. This narrative review summarizes the current discussion, the hypotheses elaborated and the algorithms depicted for the management of individuals with Lynch Syndrome on the basis of the recent data published in the literature.

To uncover the anti-tumor effects and potential mechanism of Sanwu Baisan Decoction (, SWB) in treatment of colorectal cancer (CRC) in mice.

Therapeutic effect was evaluated based on body weight gain, tumor volume, tumor growth inhibition rate, and histological changes and apoptosis in the tumor tissues. Anti-tumor immunity was studied by measuring plasma levels of anti-tumor cytokines, interleukin 6 (IL-6), interleukin 17 (IL-17), and interferon γ (IFN-γ). Gut morphological changes were evaluated by histological staining and tight junction proteins expressions. Gut microbiota composition was analyzed by 16S rRNA gene sequencing. Classical toll-like receptor 4 (TLR-4)/ cyclooxygenase 2 (COX-2)/ prostaglandin E2 (PGE-2) pathway was examined in colon tissue and tumor samples.

SWB presented high anti-tumor efficacy of CRC in mice, which manifested as decreased tumor volume and increased tumor growth inhibition rate. This anti-tumor effect of SWB was associated with elevated plasma levels of anti-tumor immune cytokines (IL-6, IL-17, and IFN-γ). Further studies showed that SWB also increases the expression of occluding and promotes the abundance of gut probiotics, , , and . Moreover, results suggested that the anti-tumor effects of SWB might associate with inducing cancer cell apoptosis and inhibiting the TLR-4/COX-2/PGE-2 pathway in both colon tissue and tumor samples.

SWB shows strong anti-tumor efficiency in mice with colorectal carcinoma, possibly through promoting the secretion of anti-tumor immune cytokines, inducing cancer apoptosis, maintaining the gut microbiota, and inhibiting tumorigenesis by inhibiting the TLR-4/COX-2/PGE-2 pathway.

Hericium erinaceus is an edible and medicinal mushroom commonly used in traditional Chinese medicine for centuries. Several studies have highlighted its therapeutic potential for gastrointestinal disorders such as gastritis and inflammatory bowel diseases. In addition, some components of this mushroom appear to possess strong antineoplastic capabilities against gastric and colorectal cancer. This review aims to analyse all available evidence on the digestive therapeutic potential of this fungus as well as the possible underlying molecular mechanisms.

A wide spectrum of metabolites (mainly, the three major nutrients and their derivatives) can be sensed by specific sensors, then trigger a series of signal transduction pathways and affect the expression levels of genes in epigenetics, which is called metabolite sensing. Life body regulates metabolism, immunity, and inflammation by metabolite sensing, coordinating the pathophysiology of the host to achieve balance with the external environment. Metabolic reprogramming in cancers cause different phenotypic characteristics of cancer cell from normal cell, including cell proliferation, migration, invasion, angiogenesis, etc. Metabolic disorders in cancer cells further create a microenvironment including many kinds of oncometabolites that are conducive to the growth of cancer, thus forming a vicious circle. At the same time, exogenous metabolites can also affect the biological behavior of tumors. Here, we discuss the metabolite sensing mechanisms of the three major nutrients and their derivatives, as well as their abnormalities in the development of various cancers, and discuss the potential therapeutic targets based on metabolite-sensing signaling pathways to prevent the progression of cancer.

Colorectal cancer (CRC) is one of the most common cancers in Western countries and remains the second most common cause of cancer death worldwide. Many studies show the importance of diet and lifestyle in the incidence of CRC, as well as in CRC prevention. However, this review summarizes those studies that analyze the impact of nutrition on tumor microenvironment modulation and cancer progression. We review the available information about the effects of specific nutrients on cancer cell progression and on the different cells within the tumor microenvironment. Diet and nutritional status in the clinical management of colorectal cancer patients are also analyzed. Finally, future perspectives and challenges are discussed, with a view to improving CRC treatments by employing nutritional approaches. These promise great benefits and will eventually improve CRC patients' survival.

Bat gut microbiomes are adapted to the specific diets of their hosts. Despite diet variation has been associated with differences in bat microbiome diversity, the influence of diet on microbial community assembly have not been fully elucidated. In the present study, we used available data on bat gut microbiome to characterize the microbial community assembly of five selected bat species (i.e., Miniopterus schreibersii, Myotis capaccinii, Myotis myotis, Myotis pilosus, and Myotis vivesi), using network analysis. These bat species with contrasting habitat and food preferences (i.e., My. capaccinii and My. pilosus can be piscivorous and/or insectivorous; Mi. schreibersii and My. myotis are exclusively insectivorous; while My. vivesi is a marine predator) offer an invaluable opportunity to test the impact of diet on bat gut microbiome assembly. The results showed that My. myotis showed the most complex network, with the highest number of nodes, while My. vivesi has the least complex structured microbiome, with lowest number of nodes in its network. No common nodes were observed in the networks of the five bat species, with My. myotis possessing the highest number of unique nodes. Only three bat species, My. myotis, My. pilosus and My. vivesi, presented a core microbiome and the distribution of local centrality measures of nodes was different in the five networks. Taxa removal followed by measurement of network connectivity revealed that My. myotis had the most robust network, while the network of My. vivesi presented the lowest tolerance to taxa removal. Prediction of metabolic pathways using PICRUSt2 revealed that Mi. schreibersii had significantly higher functional pathway's richness compared to the other bat species. Most of predicted pathways (82%, total 435) were shared between all bat species, while My. capaccinii, My. myotis and My. vivesi, but no Mi. schreibersii or My. pilosus, showed specific pathways. We concluded that despite similar feeding habits, microbial community assembly can differ between bat species. Other factors beyond diet may play a major role in bat microbial community assembly, with host ecology, sociality and overlap in roosts likely providing additional predictors governing gut microbiome of insectivorous bats.

Obesity is a complex and multifactorial problem of global importance. Additionally, obesity causes chronic inflammation, upregulates cell growth, disturbs the immune system, and causes genomic instability, increasing the risk of carcinogenesis. Colorectal cancer is one of the most common cancers, and it has become a global problem. In 2018, there were around 1.8 million new cases and around 881,000 deaths worldwide. Another risk factor of colorectal cancer associated with obesity is poor diet. A Western diet, including a high intake of red and processed meat and a low consumption of whole grains, fruits, vegetables, and fiber, may increase the risk of both colorectal cancer and obesity. Moreover, the Western diet is associated with a proinflammatory profile diet, which may also affect chronic low-grade inflammation. In fact, people with obesity often present gut dysbiosis, increased inflammation, and risk of colorectal cancer. In this article, the association between obesity and colorectal cancer is discussed, including the most important mechanisms, such as low-grade chronic inflammation, gut dysbiosis, and poor diet.