MicroRNA 93 (miR-93)

MicroRNA 93 (miR-93) is a small, non-coding RNA (approx. 22 nucleotides) in the microRNA family, encoded by the MIR93 gene located within the intron of the minichromosome maintenance 7 (MCM7) gene on chromosome 7q22[1][4]. It forms part of the miR-106b~25 cluster and acts as a key post-transcriptional regulator by binding to complementary sequences in target mRNAs, leading to mRNA degradation or inhibition of translation[4][6]. miR-93 has broad biological functions, notably in **cell cycle regulation, cell proliferation, and apoptosis**. It is dysregulated in multiple human cancers; overexpression is linked to poor prognosis, enhanced proliferation, and chemoresistance, while loss of miR-93 impairs tumor cell growth and enhances chemosensitivity[1][3][5]. Therapeutic interest centers on miR-93 both as a target for antitumor strategies (e.g., restoring its expression to combat drug resistance) and as a biomarker for disease prognosis and drug response[1][3][4]. Its direct mRNA targets include major regulators of the cell cycle (such as E2F1 and CCND1), cytoskeletal and microtubule-associated proteins (such as CRMP2 and MAPRE1), and drug efflux transporters (notably BCRP)[1][3]. Owing to its broad regulatory roles, miR-93 modulation presents both opportunities and safety concerns in therapeutic contexts.

Other names

hsa-miR-93MIR93hsa-mir-93MIRN93MIRN9miR-93microRNA-93-5pmicroRNA-93-3p

Drugs upregulate or downregulate miR-93 to influence cancer cell sensitivity. Modulation leads to altered cell proliferation, cycle arrest, and apoptosis (not direct binding, but functional interaction with drug response pathways).