MicroRNA-216b (miR-216b)

MicroRNA-216b is an evolutionarily conserved, non-coding RNA molecule, 19-24 nucleotides in length, encoded by the MIR216B gene on chromosome 2p16.1[1]. It is a member of the microRNA family, which regulates gene expression at the post-transcriptional level via base-pairing with complementary sequences in target messenger RNAs, resulting in mRNA cleavage, destabilization, or translation inhibition[7][9]. In normal and cancerous tissues, microRNA-216b acts mainly as a tumor suppressor, with reduced expression associated with increased tumor proliferation, invasion, and poor prognosis in various human cancers including non-small cell lung cancer, breast cancer, pancreatic cancer, hepatocellular carcinoma, and glioma[1][2][3][4][5]. Mechanistically, microRNA-216b directly targets several oncogenic proteins, such as SOX9, HK2, histone deacetylase 8, TPT1, and others, modulating key cancer-related cellular processes like the mTOR signaling pathway, cell cycle, apoptosis, migration, invasion, and autophagy[1][3][5]. Its levels in blood and tissues are under investigation as biomarkers for early detection, prognosis, and therapy monitoring[2][8][10]. Therapeutic strategies are being developed to restore its function using miRNA mimics or antagonists for treatment of specific cancers, though clinical application faces challenges typical of RNA-based drugs, such as delivery and safety concerns[2][10].

Other names

miR-216bmiR-216b-5pMIR216B (gene symbol)

Drugs or experimental therapeutics targeting microRNA-216b act by either mimicking its tumor-suppressive activity (miRNA mimic) or inhibiting its function (antagomir), influencing downstream cell cycle, proliferation, and apoptosis pathways