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A number of factors aid the migration and invasion of malignant cancer cells. Epithelial\u2010to\u2010mesenchymal transition (EMT), which greatly facilitates the dissemination of cancer cells, is characterized by the loss of epithelial markers and the acquisition of mesenchymal markers thereby rendering the cells more migratory and invasive. We have previously shown that the class III lysine deacetylase SIRT1 plays a critical role curbing the metastasis of ovarian cancer cells partly by blocking EMT. Here we investigated the mechanism by which SIRT1 regulates the transcription of Claudin 5 (CLDN5), an epithelial marker gene, in ovarian cancer cells. SIRT1 activation or over\u2010expression up\u2010regulated CLDN5 expression while SIRT1 inhibition or depletion down\u2010regulated CLDN5 expression. SIRT1 interacted with and deacetylated Kruppel\u2010like factor 4 (KLF4), a known transcriptional activator for CLDN5. Deacetylation by SIRT1 promoted nuclear accumulation of KLF4 and enhanced the binding of KLF4 to the CLDN5 promoter in the nucleus. SIRT1\u2010mediated up\u2010regulation of CLDN5 was abrogated in the absence of KLF4. In accordance, KLF4 depletion by siRNA rendered ovarian cancer cells more migratory and invasive despite of SIRT1 activation or over\u2010expression. In conclusion, our data suggest that SIRT1 activates CLDN5 transcription by deacetylating and potentiating KLF4.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcb.26404","type":"journal-article","created":{"date-parts":[[2017,9,9]],"date-time":"2017-09-09T09:42:41Z","timestamp":1504950161000},"page":"2418-2426","source":"Crossref","is-referenced-by-count":30,"title":["SIRT1 deacetylates KLF4 to activate Claudin\u20105 transcription in ovarian cancer cells"],"prefix":"10.1002","volume":"119","author":[{"given":"Xinjian","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Pathophysiology Nanjing Medical University Nanjing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Junliang","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pathophysiology Wuxi College of Medicine, Jiangnan University Nanjing Jiangsu 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