microRNA 595 (miR-595)

microRNA 595 (miR-595) is a short (20–24 nt) non-coding RNA molecule in the human genome that regulates post-transcriptional gene expression primarily by binding to target mRNAs and promoting translational inhibition or mRNA degradation[1]. It is transcribed by RNA polymerase II, processed by Drosha and Dicer, and incorporated into the RNA-induced silencing complex (RISC)[1][3]. miR-595 is multifunctional, implicated both in cancer and non-cancerous diseases. It acts context-dependently as a tumor promoter (glioblastoma) or tumor suppressor (ovarian and hepatocellular carcinoma, NSCLC) by targeting genes like SOX7, ABCB1, and LYRM5[1][4][5][7]. Loss or gain of miR-595 affects cell proliferation, invasion, autophagy, and chemosensitivity[1]. miR-595 level is altered in certain cancers and inflammatory conditions, serving as a non-invasive biomarker and phenotypic marker for drug response and resistance (e.g. to methotrexate and cisplatin)[1][4]. It is also involved in RNA regulatory networks as a target and modulator (e.g., circPTN/miR-595/LYRM5 axis in NSCLC, modulating angiogenesis)[5][7]. Its multifunctionality and context-specific actions make it a promising, although complex, target for novel diagnostics and therapeutics.

Other names

hsa-miR-595MIR595MIRN595hsa-mir-595

miR-595 regulates expression of genes involved in drug uptake and resistance (e.g., SLC19A1/RFC1 in methotrexate response, ABCB1 in chemosensitivity, LYRM5 in NSCLC)[1][4][7]. Modulation of tumor suppressor genes (e.g., SOX7). Inhibition or enhancement of signaling pathways (e.g., NF-κB pathway). Regulation of ribosomal integrity via RPL27A/p53 axis.