Hepatocellular carcinoma (HCC) is a highly heterogeneous and complex cancer influenced by both the tumor microenvironment and multi-level regulation of the nervous system. Increasing evidence highlights critical roles of the central nervous system (CNS) and peripheral nervous system (PNS) in modulating HCC progression. Psychological stress and emotional disturbances, representing CNS dysregulation, directly accelerate tumor growth, metastasis, and impair anti-tumor immunity in HCC. PNS involvement, particularly autonomic innervation, extensively reshapes the hepatic tumor microenvironment. Specifically, sympathetic activation promotes immune suppression, tumor cell proliferation, epithelial-mesenchymal transition (EMT), and cancer stemness via β-adrenergic signaling and hypoxia-inducible factor 1-alpha (HIF-1α) stabilization, whereas parasympathetic signals generally exert anti-inflammatory and tumor-suppressive effects mediated by acetylcholine. Neurotransmitters including epinephrine, norepinephrine, dopamine, serotonin, and acetylcholine precisely regulate critical pathways such as AKT/mTOR, ERK, and NF-κB, thereby driving malignant cell behaviors, immune evasion, and chemoresistance. Neuro-targeted pharmacological interventions (e.g., SSRIs, β-blockers, dopamine antagonists) and behavioral therapies have shown efficacy in preclinical studies, underscoring their therapeutic potential. Additionally, neural-associated biomarkers like NEDD9, CNTN1, and nerve growth factor (NGF) exhibit prognostic significance, supporting their future clinical application. By systematically integrating neuroscience with oncology, this review identifies innovative neural-based therapeutic strategies, highlights key mechanistic insights, and outlines promising directions for future research and personalized clinical management of HCC.

Most aspects of physiology and behaviour fluctuate every 24 h in mammals. These circadian rhythms are orchestrated by an autonomous central clock located in the suprachiasmatic nuclei that coordinates the timing of cellular clocks in tissues throughout the body. The critical role of this circadian system is emphasized by increasing evidence associating disruption of circadian rhythms with diverse pathologies. Accordingly, mounting evidence suggests a bidirectional relationship where disruption of rhythms by circadian misalignment may contribute to liver diseases while liver diseases alter the central clock and circadian rhythms in other tissues. Therefore, liver pathophysiology may broadly impact the circadian system and may provide a mechanistic framework for understanding and targeting metabolic diseases and adjust metabolic setpoints.

Lifestyle choices, such as dietary patterns and sleep duration, significantly impact the health of the digestive system and may influence the risk of mortality from digestive system cancer.

This study aimed to examine the associations between sleep duration, dietary habits, and mortality from digestive system cancers. The analysis included 406,584 participants from the UK Biobank cohort (54.1% women; age range: 38-73 years), with sleep duration classified as short (≤ 6 h, 24.2%), normal (7-8 h, 68.4%), and long (≥ 9 h, 7.4%). Healthy eating habits were defined as a daily intake of at least 25 g of fibre, seven portions of fruits and vegetables, and fewer than four servings of meat per week. These dietary factors were combined into a score ranging from 0 (least healthy) to 3 (healthiest). Cox proportional hazards regression analyses were conducted, with a median follow-up period of 12.6 years, ending on September 30, 2021.

3949 participants died from cancer of the digestive system. Both short and long sleep duration were associated with an increased risk of mortality from cancer of the digestive system (1.09 (1.01-1.18) and 1.14 (1.03-1.27), respectively). Additionally, a diet score ≥ 1 was linked to a lower cancer risk (0.72-0.91 (0.59-0.96)). Adjusting for smoking, type 2 diabetes, and body mass index (BMI) status eliminated the association between sleep duration and digestive cancer mortality. The association between healthy dietary patterns and the risk of digestive system cancer mortality did not vary by sleep duration.

Aberrant sleep durations may increase the risk of mortality from digestive system cancer, potentially through smoking, higher BMI, and type 2 diabetes. However, aberrant sleep durations do not seem to reduce the protective effects of a healthy dietary pattern.

This meta-analysis aims to assess the association between adult nap duration and risk of all-cause mortality and cardiovascular diseases (CVD).

PubMed, Cochrane Library, Embase and Web of Science databases were searched to identify eligible studies. The quality of observational studies was assessed using the Newcastle-Ottawa Scale. We performed all statistical analyses using Stata software version 14.0. For the meta-analysis, we calculated hazard ratio (HR) and their corresponding 95% confidence intervals (CIs). To assess publication bias, we used a funnel plot and Egger's test.

A total of 21 studies involving 371,306 participants revealed varying methodological quality, from moderate to high. Those who indulged in daytime naps faced a significantly higher mortality risk than non-nappers (HR: 1.28; 95% CI: 1.18-1.38; I2 = 38.8%; P<0.001). Napping for less than 1 hour showed no significant association with mortality (HR: 1.00; 95% CI: 0.90-1.11; I2 = 62.6%; P = 0.971). However, napping for 1 hour or more correlated with a 1.22-fold increased risk of mortality (HR: 1.22; 95% CI: 1.12-1.33; I2 = 40.0%; P<0.001). The risk of CVD associated with napping was 1.18 times higher than that of non-nappers (HR: 1.18; 95% CI: 1.02-1.38; I2 = 87.9%; P = 0.031). Napping for less than 1 hour did not significantly impact CVD risk (HR: 1.03; 95% CI: 0.87-1.12; I2 = 86.4%; P = 0.721). However, napping for 1 hour or more was linked to a 1.37-fold increased risk of CVD (HR: 1.37; 95% CI: 1.09-1.71; I2 = 68.3%; P = 0.007).

Our meta-analysis indicates that taking a nap increases the risk of overall mortality and CVD mortality. It highlights that the long duration time of the nap can serve as a risk factor for evaluating both overall mortality and cardiovascular mortality.

Sleep problems have become a significant public health concern, affecting a large portion of the global population and have been linked to increased morbidity and mortality. The incidence of gastrointestinal (GI) cancers continues to rise, posing a substantial burden on healthcare systems worldwide. This editorial aims to delve into the impact of sleep on GI cancers, including esophageal, gastric, colorectal, hepatobiliary, and pancreatic cancer. Recent literature investigating the potential connections between GI cancers and sleep was reviewed. We considered aspects such as sleep duration, sleep disorders, and circadian rhythmicity, in order to explore the underlying mechanisms that can contribute to the development of GI cancers and propose avenues for future research.