MicroRNAs (miRNAs) are short non-coding RNAs that bind to the 3' untranslated region (3'' UTR) of target mRNAs to control gene expression post-transcriptionally. Recent indications have highlighted their important roles in a variety of pathophysiological conditions as well as human malignancies. Dysregulated miRNAs act as tumor suppressor genes or oncogenes in a variety of cancers. MiR-491 has been shown to have a major effect on tumorigenesis in multiple malignancies through binding to specific genes and signaling cascades, thereby preventing cancer progression. This review provides an overview of miR-491 expression in regulatory mechanisms and biological procedures of tumor cells, as well as the prospective possible treatment effects of various types of human cancers.
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http://dx.doi.org/10.1089/dna.2022.0274 | DOI Listing |
Biomarkers
January 2025
Hacettepe University, Faculty of Medicine, Deparment of Medical Oncology, Ankara, Turkey.
Background: Dynamins are defined as a group of molecules with GTPase activity that play a role in the formation of endocytic vesicles and Golgi apparatus. Among them, DNM3 has gained recognition in oncology for its tumor suppressor role. Based on this, the aim of this study is to investigate the effects of the DNM3 gene in patients diagnosed with pancreatic cancer using bioinformatics databases.
View Article and Find Full Text PDFCell Rep
January 2025
Masonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA; Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN 55455, USA. Electronic address:
Localized prostate cancer can be cured by radiation or surgery, but advanced prostate cancer continues to be a clinical challenge. Altered alternative polyadenylation occurs in numerous cancers and can downregulate tumor-suppressor genes and upregulate oncogenes. We found that the cleavage and polyadenylation specificity factor (CPSF) complex factor CPSF1 is upregulated in patients with advanced prostate cancer, with high CPSF1 expression correlating with worse progression-free survival.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Zhongda Hospital, School of Life Sciences and Technology, Advanced Institute for Life and Health, Southeast University, Nanjing 210096, China.
Heterogeneous roles of complement C3 have been implicated in tumor metastasis and are highly context dependent. However, the underlying mechanisms linking C3 to tumor metastasis remain elusive in renal cell carcinoma (RCC). Here, we demonstrate that C3 of RCC cell-derived extracellular vesicles (EVs) contributes to metastasis via polarizing tumor-associated macrophages (TAMs) into the immunosuppressive phenotype and recruiting polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs).
View Article and Find Full Text PDFMol Biol Rep
January 2025
Department of Biochemistry, All India Institute of Medical Sciences, Jodhpur, Rajasthan, 342005, India.
Background: Differential DNA methylation in the promoter region of tumour suppressor genes leads to gene function silencing.
Materials And Methods: In this study, we aimed to evaluate the salivary promoter methylation of EDNRB, MGMT and TIMP3 genes in H&NC patients (n = 100), premalignant lesions patients (n = 25) and healthy controls (n = 50). Blood and saliva samples were collected from all three groups and 20 concomitant tumour tissues were collected from the H&NC patients.
Cell Mol Life Sci
January 2025
Institute of Endotypes in Oncology, Metabolism, and Immunology, National Research Council, Via Pietro Castellino 111, Naples, Italy.
Breast cancer represents the primary cause of death of women under 65 in developed countries, due to the acquisition of multiple drug resistance mechanisms. The PI3K/AKT pathway is one of the major regulating mechanisms altered during the development of endocrine resistance and inhibition of steps in this signalling pathway are adopted as a key strategy to overcome this issue. ADP-ribosylation is a post-translational modification catalysed by PARP enzymes that regulates essential cellular processes, often altered in diseases.
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