MicroRNA 103a-1 (miR-103a-1)

MicroRNA 103a-1 is a small, non-coding RNA (approximately 22 nucleotides) that functions in the regulation of gene expression by binding to target mRNAs and inhibiting their translation or promoting their degradation. It is transcribed as part of a capped and polyadenylated primary transcript, processed to a precursor (~70 nt hairpin), and further cleaved to the mature form by Dicer. miR-103a-1 plays significant roles in cell proliferation, glucose metabolism, migration, and inhibition of cell death, and is highly expressed in several cancers including hepatocellular carcinoma and bladder cancer, where its expression correlates with prognosis. It also directly regulates SLC23A1, the sodium-dependent vitamin C transporter, in intestinal epithelial cells. Genetic variants affecting miR-103a-1 can modulate its expression, potentially impacting disease susceptibility and progression. miR-103a-1 is encoded in the human genome and is affiliated with the miRNA class of regulatory RNAs. miR-103a-1 upregulation drives cell proliferation, migration, invasion, and glucose metabolism in tumors. miR-103a-1 interacts with key metabolic and growth genes (such as ATP11A, EIF5, ADAM10), influencing disease processes. Genetic SNPs in miR-103a-1 can dramatically affect its levels and subsequent regulatory outcomes. Elevated circulation levels of miR-103a-3p are useful for noninvasive cancer diagnostics. As a therapeutic target, it is under experimental investigation for roles in cancer and cardiovascular disease, with no clinically approved drugs directly targeting miR-103a-1.

Other names

hsa-mir-103a-1hsa-mir-103-1MIR103-1MIRN103-1mir-103a-1microRNA 103-1MIR103A1

Drugs or molecules modulating miR-103a-1 would alter its interaction with target mRNAs, modifying gene expression at the post-transcriptional level. Antagomirs (miRNA inhibitors) or mimics could be used experimentally