MicroRNA 3651 (MIR3651)

MicroRNA 3651 (MIR3651) is a short, non-coding RNA molecule (~20–24 nucleotides) that regulates gene expression post-transcriptionally, typically by binding to complementary sequences within target messenger RNAs (mRNAs) and inducing translational inhibition or mRNA degradation. MIR3651 is significantly overexpressed in several malignancies, notably colorectal and breast cancers. Its oncogenic function includes promoting cell proliferation and inhibiting apoptosis, partly via downregulation of target genes such as T-box transcription factor 1 (TBX1) in colorectal cancer and FRMD3 in breast cancer[1][8]. MIR3651 has value as a prognostic biomarker, with elevated expression associated with poorer local control and increased recurrence risk in breast cancer. Therapeutic strategies may involve miRNA inhibition or mimicry, but these approaches face hurdles such as targeting specificity, delivery, and safety due to the miRNA’s pleiotropic effects[2]. No approved drugs directly target MIR3651, but its role in cancer makes it a candidate target for future RNA-based therapeutics. MIR3651 is an endogenous gene product in humans, referenced by HGNC: 38897, NCBI Gene: 100500918, Ensembl: ENSG00000281156, and miRBase: hsa-mir-3651. Disease associations extend beyond cancer to polycystic kidney disease type 4, but cancer relevance is best documented. Biological mechanisms are consistent with those described for microRNAs generally: initial transcription as a pri-miRNA, processing to a pre-miRNA, and generation of mature miRNA that incorporates into the RNA-induced silencing complex (RISC), targeting mRNAs for repression. MIR3651’s downstream targets include TBX1 (colorectal cancer) and FRMD3 (breast cancer), where its activity leads to activation or repression of oncogenic signaling pathways, such as PI3K/AKT and MAPK/ERK. No current small molecules, antibodies, or other classic drugs are described in the literature as targeting MIR3651 specifically.

Other names

hsa-miR-3651mir-3651hsa-mir-3651MIR3651

Not applicable (microRNAs themselves are regulated by inhibitors or mimic strategies rather than classic small-molecule mechanisms; synthetic oligonucleotides could antagonize or mimic miRNA function[2])