MicroRNA 1275 (miR-1275)

MicroRNA 1275 (miR-1275) is a small, non-coding RNA molecule (microRNA) that regulates gene expression post-transcriptionally by targeting mRNAs for degradation or translational repression. It is transcribed as part of a primary microRNA transcript, processed to a precursor hairpin, and finally to a mature microRNA that is loaded into the RNA-induced silencing complex (RISC)[3][4]. miR-1275 has been shown to play versatile roles in various physiological and pathological contexts, particularly in cancer biology. In breast cancer, it acts as a tumor suppressor, with decreased expression associated with enhanced tumor growth, invasion, and resistance to apoptosis by upregulating target genes such as DVL3, PPP2R2D, THSD4, CREB1, SYT7, and PRKACA[1]. In lung adenocarcinoma, it acts as an oncomiR, maintaining cancer stem cell-like phenotypes through activation of the Wnt/β-catenin and Notch signaling pathways by repressing negative regulators like DKK3, SFRP1, GSK3B, RUNX3, and NUMB[2]. Beyond cancer, miR-1275 has been implicated as a biomarker in multiple sclerosis, cardiovascular diseases, and autoimmune diabetes, reflecting its broad significance in gene regulatory networks[5].

Other names

MIR1275hsa-mir-1275mir-1275MIRN1275

Post-transcriptional inhibition of target gene expression by binding to complementary sequences in mRNA, leading to mRNA degradation or translational repression (canonical microRNA mechanism). In experimental settings, use of miR-1275 mimics or inhibitors modulates cellular pathways (proliferation, stemness, apoptosis).