Bladder cancer (BCa) is a prevalent urogenital malignancy, imposing a significant burden on health-care systems worldwide. Long noncoding RNAs (lncRNAs) are important regulators of carcinogenesis and affect BCa progression. In this study, the influence of lncRNA LINC00115 on malignant behavior of BCa cells were explored. Bioinformatics method was used for prediction of gene expression and downstream molecules of LIN00115. LINC00115 expression level in BCa cells was measured using RT-qPCR. After LINC00115 depletion, the proportion of viable, proliferative, and apoptotic BCa cells were calculated by methyl thiazolyl tetrazolium (MTT) assays, colony formation assays, and TUNEL staining, respectively. FISH was performed to verify the cellular distribution of LINC00115. The interaction between LINC00115 and miR-4701-5p and the binding between miR-4701-5p and P4HB were confirmed using RNA pulldown, RNA immunoprecipitation (RIP), and luciferase reporter assays. Experimental results showed that LINC00115 was highly expressed in BCa cells. The silencing of LINC00115 restrained BCa cell proliferation and stimulated apoptosis. LINC00115 could directly bind to miR-4701-5p and thus initiate P4HB upregulation in BCa cells. P4HB 3'untranslated region could be targeted by miR-4701-5p. Additionally, Amplification of P4HB expression offset the effects of LINC00115 knockdown on BCa cell proliferative and apoptotic behaviors. In conclusion, LINC00115 facilitates BCa cell growth and inhibits apoptosis via interaction with miR-4701-5p and upregulation of P4HB.

A lack of effective delivery methods has hampered the study of therapeutics targeting miR-875-5p for breast cancer (BC).

The miR-875-5p mimic was conjugated to AuNPs to produce AuNP-miR-875-5p. Then, the effect of AuNP-miR-875-5p on the proliferative, migratory, invasive activities, and apoptosis of BC cells was detected, as well as on tumor growth in animals. The involvement of the MTDH/PTEN/AKT pathway in miR-875-5p-mediated BC progression was identified.

AuNP-miR-875-5p was delivered to BC cells and hampered cell malignancy. MTDH was targeted by miR-875-5p. MTDH expression was negatively correlated with miR-875-5p expression in BC tissues. The anti-tumor effect of AuNP-miR-875-5p in BC cells was counteracted by MTDH overexpression. AuNP-miR-875-5p enhanced PTEN protein expression, thereby inhibiting AKT activation by targeting MTDH. AuNP-miR-875-5p blocked MCF-7 tumor growth in vivo.

AuNPs can deliver miR-875-5p to BC cells, and AuNP-miR-875-5p has clinical potential for treating unresectable BC.

As the primary microtubule organizing center in animal cells, centrosome abnormalities are involved in human colon cancer.

To explore the role of centrosome-related genes (CRGs) in colon cancer.

CRGs were collected from public databases. Consensus clustering analysis was performed to separate the Cancer Genome Atlas cohort. Univariate Cox and least absolute shrinkage selection operator regression analyses were performed to identify candidate prognostic CRGs and construct a centrosome-related signature (CRS) to score colon cancer patients. A nomogram was developed to evaluate the CRS risk in colon cancer patients. An integrated bioinformatics analysis was conducted to explore the correlation between the CRS and tumor immune microenvironment and response to immunotherapy, chemotherapy, and targeted therapy. Single-cell transcriptome analysis was conducted to examine the immune cell landscape of core prognostic genes.

A total of 726 CRGs were collected from public databases. A CRS was constructed, which consisted of the following four genes: TSC1, AXIN2, COPS7A, and MTUS1. Colon cancer patients with a high-risk signature had poor survival. Patients with a high-risk signature exhibited decreased levels of plasma cells and activated memory CD4+ T cells. Regarding treatment response, patients with a high-risk signature were resistant to immunotherapy, chemotherapy, and targeted therapy. COPS7A expression was relatively high in endothelial cells and fibroblasts. MTUS1 expression was high in endothelial cells, fibroblasts, and malignant cells.

We constructed a centrosome-related prognostic signature that can accurately predict the prognosis of colon cancer patients, contributing to the development of individualized treatment for colon cancer.

MicroRNA-875-5p (miR-875-5p) is a cancer-related microRNA. It has been demonstrated that miR-875-5p participates in the development of various types of cancer such as hepatocellular carcinoma, gastric carcinoma, prostate and bladder cancer. Previous research suggested that miR-875 is implicated in the development of cervical cancer cells. However, the exact role and function of miR-875-5p in cervical cancer remain unexplored. It is important to examine the role and function of miR-875-5p and the associated signaling pathway, as the findings may have diagnostic and therapeutic significance. Thus, in this study, we investigated the effect of miR-875-5p on the growth and metastasis of cervical cancer cells and the possible underlying mechanisms.

Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-875-5p in cervical cancer cells and normal cervical epithelium. After overexpression or co-expression of miR-875-5p in cells, the changes in cell function were analyzed. Western blot was used to detect the expression changes of epithelial-mesenchymal transition (EMT) -related proteins and autophagy-related proteins.

Functional studies demonstrated that miR-875-5p overexpression significantly inhibited the proliferation, migration, invasion, and EMT, and promotes apoptosis and autophagy of cervical cancer cells., while miR-875-5p knockdown promoted the proliferation, migration, invasion, and EMT, and inhibited apoptosis and autophagy cervical cancer cells. Furthermore, Western blot results showed that overexpression of miR-875-5p downregulated the expressions of N-cadherin, Snail, Vimentin and microtubule-associated protein 1 light chain 3B I (LC3B I). Conversely, miR-875-5p upregulated the expression of E-cadherin.

In conclusion, our findings suggest that miR-875-5p functions as a tumor inhibitor suppressing the growth and metastasis of cervical cancer. Overexpression of miR-875-5p inhibits malignant behavior and promotes autophagy and apoptosis in cervical cancer cells. These findings advance our understanding of the role and function of miR-875-5p in cervical cancer and could facilitate the development of early genetic markers or biomarkers and therapeutic targets for cervical cancer.