MicroRNA-602 (miR-602)

MicroRNA-602 (miR-602) is a small, non-coding RNA molecule encoded by the MIR602 gene in humans. It acts as a gene regulatory element by base-pairing with complementary sequences in messenger RNAs, primarily leading to translational repression or direct degradation of targeted transcripts. miR-602 has been shown to regulate the expression of sonic hedgehog (SHH) in chondrocytes and thus plays a role in osteoarthritis pathophysiology by inhibiting expression and downstream signaling of SHH and matrix metalloproteinase 13 (MMP-13)[1]. In the gut, miR-602 targets tumor necrosis factor receptor-associated factor 6 (TRAF6), modulating inflammatory signaling in a microbiota-dependent manner; overexpression of miR-602 prevents development of experimental inflammatory bowel disease[2]. In cancers, especially esophageal squamous cell carcinoma, miR-602 acts as a driver of cell proliferation, migration, and metastasis, in part by silencing the gene FOXK2, and is upregulated in both tumor tissue and serum; its level correlates with poor prognosis and could serve as a biomarker[4]. There are no approved drugs directly targeting miR-602, but experimental agents such as synthetic antagomirs have been used in preclinical models. Therapeutic modulation of miR-602 faces technical and safety challenges common to miRNA therapies, including off-target gene regulation and delivery issues.

Other names

MIR602hsa-mir-602MIRN602

Gene silencing by binding seed sequences in target mRNA (e.g., SHH, TRAF6, FOXK2); Suppression of protein translation; Modulation of signaling cascades (down-regulation of pro-inflammatory cytokines, cell cycle regulators)