The Multifaceted Role of miR-211 in Health and Disease
- PMID: 40867554
- PMCID: PMC12384236
- DOI: 10.3390/biom15081109
The Multifaceted Role of miR-211 in Health and Disease
Abstract
MicroRNA-211 (miR-211) is a versatile regulatory molecule that plays critical roles in cellular homeostasis and disease progression through the post-transcriptional regulation of gene expression. This review comprehensively examines miR-211's multifaceted functions across various biological systems, highlighting its context-dependent activity as both a tumor suppressor and oncogene. In physiological contexts, miR-211 regulates cell cycle progression, metabolism, and differentiation through the modulation of key signaling pathways, including TGF-β/SMAD and PI3K/AKT. miR-211 participates in retinal development, bone physiology, and protection against renal ischemia-reperfusion injury. In pathological conditions, miR-211 expression is altered in various diseases, particularly cancer, where it may be a useful diagnostic and prognostic biomarker. Its stability in serum and differential expression in various cancer types make it a promising candidate for non-invasive diagnostics. The review also explores miR-211's therapeutic potential, discussing both challenges and opportunities in developing miRNA-based treatments. Understanding miR-211's complex regulatory interactions and context-dependent functions is crucial for advancing its clinical applications for diagnosis, prognosis, and targeted therapy in multiple diseases.
Keywords: TGF-β signaling; cancer biomarkers; cellular metabolism; gene regulation; miR-211; microRNA; microRNA-211; post-transcriptional regulation; therapeutic targets.
Conflict of interest statement
The authors declare no conflicts of interest.
Figures
References
-
- Miska E.A., Alvarez-Saavedra E., Abbott A.L., Lau N.C., Hellman A.B., McGonagle S.M., Bartel D.P., Ambros V.R., Horvitz H.R. Most Caenorhabditis elegans microRNAs Are Individually Not Essential for Development or Viability. PLoS Genet. 2007;3:e215. doi: 10.1371/journal.pgen.0030215. - DOI - PMC - PubMed
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Medical
