microRNA 616 (miR-616)

microRNA 616 is a human microRNA derived from the MIR616 gene, located within the second intron of the CHOP/DDIT3 locus[1]. It functions primarily by binding to the 3′UTR or coding regions of specific mRNAs, leading to repression of their translation or destabilization. miR-616 is involved in the regulation of cell proliferation, migration, apoptosis, and cellular stress responses. It plays an oncogenic role in several human cancers by downregulating tumor suppressor genes like TFPI-2, PTEN, and SOX7, and it is implicated in resistance to androgen deprivation in prostate cancer[2][3][4]. Conversely, miR-616 may also inhibit cell proliferation via suppression of oncogenes such as c-MYC in certain contexts[1]. The dual role of miR-616—either promoting or inhibiting cancer progression—depends on the specific cancer type and cellular context. Current research examines its potential as both a biomarker and a therapeutic target, although no approved drugs directly targeting miR-616 exist to date.

Other names

MIR616hsa-mir-616MIRN616miR-616microRNA-616

Inhibition: Anti-miR-616 oligonucleotides suppress miR-616 activity, leading to restoration of target tumor suppressor genes like TFPI-2 and SOX7 and inhibition of cancer proliferation/metastasis. Overexpression: miR-616 mimics promote downregulation of oncogenes such as c-MYC and tumor suppressors in various contexts.