MicroRNA 424 (miR-424)

MicroRNA 424 (miR-424) is a short non-coding RNA (microRNA) involved in the post-transcriptional regulation of gene expression by affecting the stability and translation of target mRNAs[1][3]. It is processed from a longer precursor to a mature miRNA by nuclear and cytoplasmic RNAse enzymes (Drosha and Dicer), then incorporated into the RNA-induced silencing complex (RISC) to direct translational repression or degradation of specific mRNAs[1]. miR-424 is encoded as part of the miR-424/503 cluster, resides on the X chromosome, and belongs to the miR-16 family[4]. It plays major roles in diverse biological processes including the regulation of cell proliferation, apoptosis, differentiation, migration, angiogenesis, and development of drug resistance[2]. Aberrant expression of miR-424 is associated with various human diseases, principally multiple cancers, where it can function as either a tumor suppressor or oncogene depending on the context[2][4]. Altered miR-424 levels are clinically significant as diagnostic or prognostic biomarkers, and experimental therapeutic modulation of miR-424 is an area of active research[2][4].

Other names

hsa-miR-424MIR322MIRN424miRNA424mir-424MIR424hsa-mir-424

Experimental therapeutic approaches targeting miR-424 involve modulation of its activity. This would either enhance or inhibit its inherent mechanism of action, which includes the modulation of tumor suppressor or oncogene expression through RNA-induced silencing complex (RISC)-dependent translational inhibition or mRNA destabilization. miR-424 regulates various signaling pathways such as Wnt/β-catenin, Hippo, EGFR, and PI3K/AKT by targeting specific mRNAs like LRP6, KIF23, CHK1, Wee1, KDM5B, E2F7, DCLK1, GPER-1, SCN4B, CCNE1, AKT3, Rictor, TGFBR3, SMAD7, SOCS2, SOCS6, YAP1, c-Myb, TRIM29, ARK5, and ICAT.