MicroRNA 32 (miR-32)

MicroRNA 32 (miR-32) is an endogenous, small (approximately 22 nucleotides) non-coding RNA molecule that regulates gene expression at the post-transcriptional level by base pairing with target mRNAs and inhibiting their translation or promoting their degradation. It is transcribed from intron 14 of the TMEM245 gene (chromosome 9q31.3), with mature miRNA products hsa-miR-32-5p and hsa-miR-32-3p commonly studied in human biology[1][2][4][5]. MiR-32 is expressed in a variety of human tissues including serum, liver, kidney, breast, and brain[1]. Alterations in miR-32 expression are implicated in multiple disease processes, most notably in tumorigenesis where it can act as an oncomiR (oncogenic microRNA) in some contexts—promoting proliferation, invasion, and metastasis—or as a tumor suppressor in others[1][5][3]. In cancer, miR-32 has been associated with regulation of well-established tumor suppressor genes such as PTEN and KLF4[1][2][3]. It also plays a significant role in metabolic and cardiovascular diseases, including diabetic nephropathy, by regulating pathways involved in autophagy, fibrosis, and inflammation[1][5]. Expression of miR-32 may serve as a noninvasive disease biomarker and as a potential therapeutic target[1][4][5][6]. However, the dual and context-dependent roles of miR-32 in physiology and disease highlight important safety and therapeutic challenges for targeted intervention[1][5].

Other names

hsa-mir-32MIR32miRNA32miR-32MIRN32hsa-miR-32-5phsa-miR-32-3p