MicroRNA 106b (miR-106b)

MicroRNA 106b is a non-coding RNA molecule (miRNA) approximately 22 nucleotides in length that post-transcriptionally regulates gene expression by binding to complementary sequences in the 3′ untranslated regions (3′ UTRs) of target mRNAs, resulting in translational repression or mRNA degradation[2][3][4]. miR-106b is part of the miR-106b~25 cluster (with miR-93 and miR-25), located within an intron of the MCM7 gene[4]. It is classified as an oncomiR due to its frequent overexpression in numerous cancer types (including hepatocellular, prostate, gastric, breast, esophageal adenocarcinoma, cholangiocarcinoma, and others), where it promotes tumorigenesis by downregulating genes involved in cell cycle arrest (e.g., p21/CDKN1A), apoptosis (e.g., Bim), and other tumor suppressor pathways (e.g., PTEN, RB1, KLF family)[1][2][3][4]. miR-106b plays a central role in promoting cell proliferation, facilitating the G1-S transition of the cell cycle, inhibiting DNA damage-induced checkpoint arrest, and enhancing invasive/migratory behaviors in cancer cells[1][2][3][4]. Its dysregulation is also associated with other diseases, such as Alzheimer's disease[5]. miR-106b is considered a promising therapeutic target, and its expression levels can serve as biomarkers for cancer prognosis or stratification. However, therapeutic interventions targeting microRNAs carry potential safety risks due to the widespread and promiscuous binding of miR-106b to hundreds of mRNAs, raising challenges in specificity and safety[3][4].

Other names

hsa-miR-106bMIRN106Bmir-106bhsa-mir-106bMIR106B-5pmiRNA-106b

Inhibition of target mRNA translation; Promotion of mRNA degradation of tumor suppressor genes (e.g., p21/CDKN1A, KLF family, PTEN, RB1, E2F1, Bim/BCL2L11)