Journal
CANCER LETTERS
Volume 355, Issue 1, Pages 25-33Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2014.09.022
Keywords
Hepatocellular carcinoma; KLF9; Apoptosis; p53 protein; Transcriptional regulation
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Funding
- National Science Foundation of China [81201542, 81301716]
- Natural Science Foundation of Shanghai [12ZR1430100]
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Kruppel-like factor 9 (KLF9) is known to be a tumor suppressor gene in colorectal tumors and glioblastoma; however, the functional status and significance of KLF9 in hepatocellular carcinoma (HCC) is unclear. We report here that KLF9 is downregulated in HCC tissues. Restoration of KLF9 significantly inhibited growth and caused apoptosis in SK-Hepl and HepG2 cells. We found that KLF9 positively regulated p53 levels by directly binding to GC boxes within the proximal region of the p53 promoter. Moreover, in the presence of cycloheximide, KLF9 significantly increased p53 stability in HCC cells. Remarkably, ectopic expression of KLF9 was sufficient to delay the onset of tumors and to promote regression of the established tumors in vivo, suggesting that KLF9 plays a critical role in HCC development and that pharmacological or genetic activation of KLF9 may have potential in the treatment of HCC. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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