MicroRNA 623 (miR-623)

MicroRNA 623 (miR-623) is a human microRNA involved in the post-transcriptional regulation of gene expression, primarily through binding to the 3' untranslated regions of target mRNAs and promoting their degradation or inhibiting translation. MiR-623 is strongly associated with tumor suppressor activity; its levels are reduced in various cancers including breast, gastric, lung adenocarcinoma, and chordoma. Overexpression of miR-623 inhibits cancer cell proliferation, migration, invasion, and increases apoptosis by directly targeting molecules such as Cyclin D1 (CCND1), Cyclin-Dependent Kinase 4/6 (CDK4/6), and Ku80. In gastric cancer cells, miR-623 increases chemosensitivity to 5-Fluorouracil (5-FU) via the apoptosis pathway. Aberrant miR-623 expression may serve as a biomarker for tumor progression, prognosis, and possibly therapeutic response. miR-623 is a key regulatory microRNA, acting mainly as a tumor suppressor by targeting cell cycle and DNA repair proteins. Its therapeutic targeting is under active research, especially in cancers with chemoresistance or metastatic potential. No approved drugs directly modulate miR-623, but its restoration enhances chemosensitivity to 5-FU in preclinical models.

Other names

miR-623MIR623hsa-miR-623MIRN623

Drugs that enhance miR-623 expression may suppress cell proliferation and increase apoptosis in cancer cells. Direct targeting/downregulation of Cyclin D1 (CCND1) and Cyclin-Dependent Kinases (CDK4/6)—key regulators of the cell cycle. Inhibition of major cancer pathways: PI3K/Akt/mTOR, Wnt/β-Catenin signaling.