MicroRNA 92a (miR-92a)

MicroRNA 92a (miR-92a) is a short, single-stranded, non-protein coding RNA molecule belonging to the miR-17–92 cluster and is highly conserved across species[1][3]. It functions as a post-transcriptional regulator by binding to the 3′-untranslated regions of target mRNAs, leading to translational repression or degradation. miR-92a is broadly expressed and plays crucial roles in regulating cell proliferation, apoptosis, differentiation, and migration in both normal physiology and disease contexts[4][3][8]. Dysregulation of miR-92a has been implicated in the pathogenesis of multiple cancers, where it commonly acts as an oncogene by suppressing tumor suppressor genes—including FBXW7, PTEN, and NF2—thus promoting cell proliferation, metastasis, and resistance to apoptosis[2][5][6][9]. In the clinic, elevated circulating levels of miR-92a serve as a stable, non-invasive biomarker for early cancer diagnosis, particularly in colorectal cancer[7]. Therapeutic targeting of miR-92a, such as through miRNA inhibitors or antisense oligonucleotides, is under investigation to counter its pro-tumorigenic effects, but this approach must be balanced against potential safety concerns due to miR-92a’s regulatory breadth in normal tissues[4][8].

Other names

miR-92amiR-92a-3pmir-92microRNA-92a

Antagomirs/anti-miRs inhibit miR-92a, thereby upregulating tumor suppressor targets (e.g., FBXW7, PTEN, NF2)[2][3][5]. Therapeutic modulation of miR-92a restores or suppresses downstream gene expression, affecting cell growth and apoptosis[4][5][6].