MicroRNA 432-5p (miR-432-5p) (miR-432-5p)

MicroRNA 432-5p (miR-432-5p) is a highly conserved, small non-coding RNA that primarily functions as a tumor suppressor across various human malignancies, including colorectal, lung, and hepatocellular carcinomas (NIH, 2021). It exerts its biological effects by binding to the 3'-untranslated region (3'-UTR) of target mRNAs, such as CXCL5 and components of the Wnt/beta-catenin and TGF-beta signaling pathways, leading to post-transcriptional gene silencing (PubMed, 2020). In oncology, its downregulation is frequently associated with increased cell proliferation, migration, and invasion, while its restoration can inhibit tumorigenicity and enhance sensitivity to chemotherapy agents like cisplatin (NIH, 2021). Conversely, in estrogen receptor-positive breast cancer, elevated exosomal levels of miR-432-5p have been identified as a key mediator of acquired resistance to CDK4/6 inhibitors, such as palbociclib and ribociclib, by suppressing the TGF-beta pathway and subsequently upregulating CDK6 (NIH, 2021). Beyond its role in cancer, miR-432-5p is implicated in the pathogenesis of multiple sclerosis and is being investigated as a biomarker for embryo implantation success (Frontiers in Endocrinology, 2021). Its diverse regulatory roles and involvement in drug resistance mechanisms make it a significant target for the development of miRNA-based mimics and inhibitors in precision medicine.

Other names

hsa-miR-432-5pMIR432MicroRNA 432MIRN432MIMAT0002815hsa-mir-432

miR-432-5p functions through post-transcriptional gene silencing by binding to the 3'-untranslated region (3'-UTR) of target mRNAs, leading to their degradation or translational repression. It regulates key pathways such as Wnt/beta-catenin and TGF-beta, and its downregulation often promotes tumor progression, while its upregulation can mediate resistance to CDK4/6 inhibitors by increasing CDK6 expression.