MiR‐25 alleviates polyQ‐mediated cytotoxicity by silencing ATXN3. Issue 24 (20th November 2014)

• Record Type: Journal Article
• Authors: Huang, Fengzhen; Zhang, Li; Long, Zhe; Chen, Zhao; Hou, Xuan; Wang, Chunrong; Peng, Huirong; Wang, Junling; Li, Jiada; Duan, Ranhui; Xia, Kun; Chuang, De-Maw; Tang, Beisha; Jiang, Hong
• Is Part Of: FEBS letters. Volume 588:Issue 24(2014)
• Page Start: 4791
• Page End: 4798
• Publication Date: 2014-11-20
• Subjects: Spinocerebellar ataxia type 3/Machado–Joseph disease -- ATXN3 -- Cytotoxicity -- Neuronal intranuclear inclusion -- miR-25 -- Gene expression regulation; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1016/j.febslet.2014.11.013
• Languages: English
• ISSNs: 0014-5793

Abstract

Abstract : MicroRNAs (miRNAs) have been reported to play significant roles in the pathogenesis of various polyQ diseases. This study aims to investigate the regulation of ATXN3 gene expression by miRNA. We found that miR‐25 reduced both wild‐type and polyQ‐expanded mutant ataxin‐3 protein levels by interacting with the 3′UTR of ATXN3 mRNA. miR‐25 also increased cell viability, decreased early apoptosis, and downregulated the accumulation of mutant ataxin‐3 protein aggregates in SCA3/MJD cells. These novel results shed light on the potential role of miR‐25 in the pathogenesis of SCA3/MJD, and provide a possible therapeutic intervention for this disorder. Abstract : ATXN3 is a target of miR‐25. miR‐25 reduces ATXN3 protein levels. miR‐25 decreases polyQ‐mediated toxicity and NII formation.