MicroRNA 3195 (MIR3195)

MicroRNA 3195 is a short, non-coding RNA molecule (miRNA) involved in the post-transcriptional regulation of gene expression by binding to the 3′ untranslated regions (3′UTR) of target mRNAs, resulting in their degradation or translational repression[3]. It is upregulated in castration-resistant prostate cancer (CRPC) tissue compared to primary prostate cancer, where it may influence cell migration and invasion[1]. In prostate cancer cell models under hypoxic conditions, microRNA 3195 is upregulated in response to melatonin and mediates anti-angiogenic effects through downregulation of HIF-1α, HIF-2α, and VEGF, thereby reducing migration and angiogenesis[2]. While primarily studied in cancer contexts, especially prostate cancer and non-small cell lung cancer, its precise target genes and broader physiological roles remain under investigation[1][2][3]. MicroRNA 3195 may serve as a biomarker for disease state or therapeutic response but is not a direct drug target or receptor[1][2].

Other names

hsa-mir-3195MIR3195miRNA3195miR-3195

MicroRNA 3195, when upregulated, leads to the downregulation of angiogenesis-related genes (such as HIF-1α, HIF-2α, and VEGF). It also inhibits cell migration and invasion, as observed in prostate and lung cancer cell models.