MicroRNA 326 (miR-326)

MicroRNA 326 (miR-326) is a small, endogenous non-coding RNA that regulates gene expression primarily by binding to complementary sequences in target mRNAs, resulting in their degradation or translational repression. It functions as a tumor suppressor in various cancers, including glioma, hepatocellular carcinoma, breast cancer, and non-small cell lung cancer, by impairing cell proliferation, promoting apoptosis, and inhibiting invasion and metastasis[1][2][3][4]. In autoimmunity, miR-326 has been shown to promote B cell differentiation and autoantibody production by targeting the transcription factor Ets-1, contributing to the pathogenesis of systemic lupus erythematosus (SLE)[5]. Additionally, elevated miR-326 levels have been observed in multiple sclerosis, implicating it as a pro-inflammatory molecule and potential biomarker[5][6][7]. miR-326 exerts its biological effects via modulation of pathways such as MAPK, PI3K-AKT, Wnt/β-catenin, NGF/EGFR, and ErbB/PI3K[1][3][4].

Other names

hsa-mir-326MIRN326MIR326mir-326

Post-transcriptional gene silencing; Regulation of gene expression by targeting mRNA (e.g., NOB1, FGF1, LASP1, Ets-1)