Vimentin acetylation is involved in SIRT5-mediated hepatocellular carcinoma migration.
Year: 2018
Type: article
Abstract: , gain and loss-of-function studies were performed to evaluate the role of SIRT5 in epithelial-mesenchymal transition (EMT). Knockdown of SIRT5 promoted EMT, as indicated by the upregulation of Snail and downregulation of E-cadherin, whereas overexpression of SIRT5 decreased Snail and upregulated E-cadherin. Mechanistically, SIRT5 was found to bind to and deacetylate vimentin at lysine 120. Cell migration was enhanced by overexpression of either wild-type vimentin or acetylation mimetic vimentin (K120Q), whereas cell migration was inhibited by overexpression of the non-acetylation vimentin (K120R). Taken together, these findings indicated that downregulated SIRT5-mediated vimentin acetylation may be involved in the EMT in HCC. Better understanding of SIRT5 may lead to its clinical application as a biomarker for prognosis of prediction of prognosis, as well as a novel therapeutic target.
Source: Europe PMC (PubMed Central)
Authors: Dan Guo, Xuhong Song, Tangfei Guo, Songgang Gu, Xiaolan Chang, Ting Su, Xianghong Yang, Bin Liang, Dongyang Huang
Language: English
Subfield: Geriatrics and Gerontology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2987316548