MicroRNA 296 (miR-296)

MicroRNA 296 (miR-296) is a small, non-coding RNA molecule involved in post-transcriptional regulation of gene expression by binding target mRNAs and repressing their translation or promoting their degradation[3][1]. Its mature form is produced from a precursor hairpin through Dicer-mediated processing, and functions via association with the RNA-induced silencing complex (RISC)[3]. miR-296 is highly conserved in mammals, including humans, and is classified as an “angiomiR” due to its central role in regulating angiogenesis, particularly through modulating the VEGF pathway and related endothelial responses[3][1]. It is also implicated in diverse cellular processes such as inflammation, cell proliferation, apoptosis, macrophage polarization, and cholesterol metabolism[1]. Evidence supports its involvement in atherosclerosis, hypertension, several cancers (including osteosarcoma and gastric cancer), and metabolic and inflammatory diseases[1][2][3]. miR-296 acts mainly by targeting a range of mRNAs (e.g., HGS, p53, p21, p27, SOCS-2, NumbL, NGFR, caspase-8, ICAM-1, CX3CR1), thereby influencing critical biological and pathological processes[1][2][3]. While miR-296 is investigated as a therapeutic target and biomarker, no approved drugs specifically target it, and significant safety and specificity obstacles remain for clinical translation[1][2][3].

Other names

miR-296MIR296hsa-mir-296MIRN296miRNA296mir-296

Not applicable for classic drugs, but experimental inhibition or overexpression (via miRNA mimics, inhibitors, or antagomirs) alters disease-relevant cellular pathways such as angiogenesis (by targeting HGS, VEGF pathway), cell proliferation (by targeting p53, p21, p27), apoptosis (via NGFR, caspase-8), and inflammation (via SOCS-2, NumbL, Scrib, CX3CR1, ICAM-1)