MicroRNA 3652 (miR-3652)

MicroRNA 3652 (miR-3652) is a short (20–24 nucleotide) non-coding RNA molecule involved in post-transcriptional regulation of gene expression by affecting mRNA stability and translation[1]. Like other microRNAs, it is transcribed as a primary transcript, processed by Drosha and Dicer enzymes, and incorporated into the RNA-induced silencing complex (RISC), which binds target mRNAs mainly to suppress translation or induce degradation[1][2]. miR-3652 has been identified as downregulated in ovarian cancer, where its reduced activity is associated with upregulation of oncogenic genes such as CCNL1 (Cyclin L1), GLI2, NFIB and others, contributing to tumor proliferation, metastasis, and negative patient prognosis[3]. Its regulation of genes in the cell cycle, transcriptional control, mRNA editing, calcium influx, and oncogenic pathways suggests an important functional role, particularly in cancer biology[3]. It is being investigated as a potential diagnostic and therapeutic target in ovarian cancer due to its significant impact on tumor-associated gene networks[3].

Other names

hsa-mir-3652MIR3652

Gene expression modulation (as a drug target, the typical mechanism would be modulation of microRNA levels affecting downstream gene expression)