MicroRNA 511-5p (miR-511-5p)

miR-511-5p is a mature microRNA strand derived from the MIR511 gene, which is located within the fifth intron of the CD209 (DC-SIGN) gene. It functions as a critical post-transcriptional regulator by binding to the 3'-untranslated regions (UTRs) of target messenger RNAs, thereby inducing their degradation or inhibiting their translation [3, 9]. In the context of oncology, miR-511-5p predominantly acts as a tumor suppressor; its expression is frequently downregulated in various malignancies, including breast, colorectal, and gastric cancers [1, 2, 21]. By targeting key effectors such as CCNE1, CHEK1, and GPR116, it modulates essential cellular processes like the cell cycle, PI3K/AKT signaling, and epithelial-mesenchymal transition [1, 15, 22]. Beyond its role in cancer, miR-511-5p is involved in regulating the innate immune response through the targeting of Toll-like receptor 4 (TLR4) and has been implicated in neuronal differentiation via the regulation of FKBP5 [3, 4]. It also serves as a potential biomarker for inflammatory conditions like periodontitis and infectious diseases such as toxoplasmosis [6, 7]. Although no miR-511-5p-based therapies are currently FDA-approved, the use of miRNA mimics to restore its function is a subject of active preclinical investigation, particularly for treating cancers where its expression is lost [14, 15].

Other names

hsa-miR-511-5pMIR511microRNA 511-1microRNA 511-2miR-511

miR-511-5p acts through RNA interference (RNAi) by binding to the 3'-untranslated regions (3'-UTRs) of target mRNAs, such as TLR4, FKBP5, GPR116, PAK2, CCNE1, and CHEK1, leading to their degradation or translational repression [1, 2, 3, 4].