MicroRNA-96 (miR-96)

MicroRNA-96 (miR-96) is a small non-coding RNA molecule that plays a crucial role in the post-transcriptional regulation of gene expression by targeting specific mRNAs for degradation or translational inhibition. It is a member of the evolutionary conserved miR-183/96/182 cluster, which is essential for the development and maintenance of sensory organs, particularly the hair cells in the vertebrate inner ear. Mutations in the seed region of miR-96 are a known cause of autosomal dominant non-syndromic deafness 50 (DFNA50), highlighting its importance in auditory function. Beyond the sensory system, miR-96 is frequently dysregulated in various cancers, where it often functions as an oncomiR by downregulating tumor suppressors like FOXO1 to promote cell proliferation and survival. Because of its specific role in disease pathology, miR-96 is a target for therapeutic intervention using antisense oligonucleotides (antagomirs) and novel small molecules designed to inhibit its biogenesis. Its presence in biofluids also makes it a promising candidate for use as a non-invasive biomarker in oncology.

Other names

hsa-mir-96MIR96MicroRNA 96miR-183-96-182 cluster member

MicroRNA-96 functions by binding to the 3' untranslated region (UTR) of target messenger RNAs (mRNAs), leading to translational repression or mRNA degradation. In cancer, it often acts as an oncomiR by silencing tumor suppressor genes such as FOXO1, RECK, and SAMD9. In the auditory system, it regulates a network of genes essential for the maturation and survival of sensory hair cells.