Abstract:
:KLF5 is a transcription factor that plays important roles in multiple physical and pathological processes, including cell growth, cell cycle regulation, and angiogenesis. To better characterize KLF5 function in bladder carcinogenesis, we established stable TSU-Pr1 cell clones expressing different levels of KLF5. These clones were then characterized for cell growth, cell cycle progression, tumorigenesis, and alteration in gene expression. Overexpression of KLF5 promoted tumorigenesis of the TSU-Pr1 cancer cells in mice. Consistently, KLF5 increased G1 to S phase transition, which was accompanied by the upregulation of cyclin D1, phosphorylation of MAPK and Akt, and reduced protein levels for CDK inhibitors p27 and p15. Microarray analysis combined with expression verification in different cell systems identified a number of additional genes that are potentially regulated by KLF5, including HBP17, ITGA6, and RAIG1. These findings suggest that the KLF5 transcription factor plays an oncogenic role in the TSU-Pr1 bladder cancer cell line through the regulation of a subset of genes.
journal_name
Int J Cancerjournal_title
International journal of cancerauthors
Chen C,Benjamin MS,Sun X,Otto KB,Guo P,Dong XY,Bao Y,Zhou Z,Cheng X,Simons JW,Dong JTdoi
10.1002/ijc.21533keywords:
subject
Has Abstractpub_date
2006-03-15 00:00:00pages
1346-55issue
6eissn
0020-7136issn
1097-0215journal_volume
118pub_type
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