microRNA 2355 (miR-2355 (or miR-2355-5p/miR-2355-3p for strand specification))

microRNA 2355 (miR-2355) is a small, evolutionarily conserved non-coding RNA molecule in humans, part of the microRNA family, that modulates gene expression at the post-transcriptional level by binding mainly to the 3' untranslated region of target mRNAs, thereby promoting translational repression or mRNA degradation[1][2][3]. It exists as two principal mature strands, miR-2355-5p and miR-2355-3p. miR-2355-5p is implicated in promoting tumor cell proliferation, cell cycle progression, migration, and angiogenesis in clear cell renal cell carcinoma (ccRCC), and its loss leads to reduced cell proliferation, impaired angiogenesis, S-phase cell cycle arrest, and tumor growth inhibition[1]. It directly or indirectly regulates several tumor suppressor genes such as ACO1, BTG2, CMTM4, SLIT2, and WDFY2, and interacts with components of the VHL/HIF-2α pathway, suggesting its role in hypoxia-driven oncogenic signaling[1]. Previous studies have also reported miR-2355 dysregulation in various cancer types, where it can function as either a tumor suppressor or oncogene, depending on cellular context[1][4]. miR-2355-3p, a specific mature product, has potential as a biomarker in lung adenocarcinoma (LUAD) and possibly other cancers due to its distinctive expression profile[4]. No current drugs are approved to target miR-2355 directly, but antisense technologies are under exploration in the miRNA field.

Other names

hsa-miR-2355miR-2355hsa-mir-2355MIR2355miR-2355-5pmiR-2355-3p

Antisense inhibition (e.g., using anti-miR oligonucleotides to block miR-2355 function); RNA interference mechanisms: binding leads to mRNA degradation or translational repression