microRNA 106a (miR-106a)

microRNA 106a (miR-106a) is a member of the miR-17 family located on chromosome Xq26.2, encoded by the MIR106A gene[4]. It functions as a short (20–24 nt), non-coding RNA involved in post-transcriptional gene regulation by binding to complementary sequences in the 3′-UTR of target mRNAs, leading to mRNA degradation or translational inhibition through the RNA-induced silencing complex (RISC)[4]. miR-106a plays roles in regulating cell cycle, apoptosis, autophagy, immune response, and cell proliferation, and is extensively studied for its involvement in the development and progression of various cancers, as well as for its role in drug resistance (notably multidrug resistance in chemotherapy)[2][3][4]. Additionally, miR-106a modulates immune responses during infection (e.g., tuberculosis) by targeting autophagy-related genes (ULK1, ATG7, ATG16L1)[1]. miR-106a is a promising diagnostic and prognostic biomarker and a potential therapeutic target, though miRNA-based therapies are still experimental and require careful consideration of broad regulatory impacts and safety[3][4].

Other names

MIR106Amir-106aMIRN106Ahsa-mir-106amir-106

Drugs mimicking miR-106a may suppress target gene expression (such as E2F1, PTEN, ULK1, ATG7, ATG16L1). Inhibitors (antagomiRs) restore expression of target genes and enhance processes such as autophagy or apoptosis. Modulation of cell proliferation, apoptosis, autophagy, and drug resistance by regulating signaling pathways (e.g., PTEN/Akt, caspases, RUNX3, ABC transporters).