MicroRNA 299 (MIR299)

MicroRNA 299 (MIR299) is a small, non-coding RNA molecule of the microRNA class found in humans, transcribed as part of a primary miRNA and processed to its mature form (miR-299-3p and miR-299-5p)[1][5][7]. It regulates gene expression at the post-transcriptional level by binding to complementary sequences in the 3′ UTR of target mRNAs, thereby suppressing translation or promoting mRNA degradation[1]. MIR299 plays diverse biological roles, including inhibition of cell proliferation, metastasis, and angiogenesis in various cancers, modulation of androgen receptor and VEGFA signaling pathways, regulation of autophagy and apoptosis in neuronal cells, and involvement in chemoresistance in tumor tissues[2][3][4][6][8]. It has been investigated as a potential biomarker in neurodegenerative disorders such as Alzheimer’s disease and several cancers, where its altered expression is associated with disease state and therapy response[3][4][6][8]. Potential therapeutic strategies targeting MIR299 include mimics or inhibitors (antagomiRs) aimed at restoring its normal expression or silencing overactive pathways[3][6][8].

Other names

hsa-mir-299MIRN299mir-299miR-299-5pmiR-299-3p

Mimic or antagomiR therapies: AgomiR-299-5p delivery reduces autophagy and apoptosis, providing neuroprotection[3] Regulation of resistance and sensitivity to chemotherapy by affecting cell cycle/apoptosis gene expression[8][6] Inhibition of oncogenic signaling pathways (androgen receptor, VEGFA, EMT regulators)[4][6]