KLF8 is required for bladder cancer cell proliferation and migration. (18th January 2015)

• Record Type: Journal Article
• Authors: Liang, Kai; Liu, Tao; Chu, Ning; Kang, Jian; Zhang, Rui; Yu, Yong; Li, Dongqi; Lu, Dexiang
• Is Part Of: Biotechnology and applied biochemistry. Volume 62:Number 5(2015)
• Page Start: 628
• Page End: 633
• Publication Date: 2015-01-18
• Subjects: Biotechnology -- Periodicals; Biochemical engineering -- Periodicals; Biochemistry -- Periodicals; Biochemistry -- Periodicals; Genetic Techniques -- Periodicals; Microbiological Techniques -- Periodicals; 660.6
• DOI: 10.1002/bab.1310
• Languages: English
• ISSNs: 0885-4513

Abstract

<abstract abstract-type="main"> <title>Abstract</title> <p>Krüppel‐like factor 8 (KLF8) belongs to the Sp/KLF family of transcription factors. Recently, it is affirmed that KLF8 plays an important role in the regulation of epithelial–mesenchymal transition, which is a key process that occurs during cancer metastasis. Although the overexpression of KLF8 has been observed in several types of human cancers, the functional role of KLF8 in human bladder cancer remains unknown. Here, we investigated the effects of KLF8 knockdown on bladder cancer cell proliferation and migration <italic>in vitro</italic>. Lentivirus‐mediated small interfering RNA (siRNA) targeting KLF8 specifically downregulated its expression in T24 and BT5637 bladder cancer cells. Knockdown of KLF8 significantly inhibit cell proliferation and colony formation. Cell cycle analysis showed that knockdown of KLF8 arrested T24 cells in the G0/G1 phase. Moreover, cell migration was attenuated in T24 cells after KLF8 knockdown. Furthermore, knockdown of KLF8 resulted in a reduction in vimentin and N‐cadherin expression and an increase in β‐catenin expression. These results indicate that KLF8 plays a crucial role in proliferation and migration of bladder cancer cells, and inhibition of KLF8 by siRNA may provide a potential therapeutic approach for gene therapy in bladder cancer.</p> </abstract>