Publication in detail

Mol Cell Biol. 2013 Dec;33(24):4919-35. doi: 10.1128/MCB.00787-13. Epub 2013 Oct 14.

KLF5 activates microRNA 200 transcription to maintain epithelial characteristics and prevent induced epithelial-mesenchymal transition in epithelial cells.

Zhang, B; Zhang, Z; Xia, S; Xing, C; Ci, X; Li, X; Zhao, R; Tian, S; Ma, G; Zhu, Z; Fu, L; Dong, JT

Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin, China.

Abstract:
KLF5 is an essential basic transcriptional factor that regulates a number of physiopathological processes. In this study, we tested whether and how KLF5 modulates the epithelial-mesenchymal transition (EMT). Using transforming growth factor β (TGF-β)- and epidermal growth factor (EGF)-treated epithelial cells as an established model of EMT, we found that KLF5 was downregulated during EMT and that knockdown of KLF5 induced EMT even in the absence of TGF-β and EGF treatment, as indicated by phenotypic and molecular EMT properties. Array-based screening suggested and biochemical analyses confirmed that the microRNA 200 (miR-200) microRNAs, a group of well-established EMT repressors, were transcriptionally activated by KLF5 via its direct binding to the GC boxes in miR-200 gene promoters. Functionally, overexpression of miR-200 prevented the EMT induced by KLF5 knockdown or by TGF-β and EGF treatment, and ectopic expression of KLF5 attenuated TGF-β- and EGF-induced EMT by rescuing the expression of miR-200. In mouse prostates, knockout of Klf5 downregulated the miR-200 family and induced molecular changes indicative of EMT. These findings indicate that KLF5 maintains epithelial characteristics and prevents EMT by transcriptionally activating the miR-200 family in epithelial cells.

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