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Carcinogenesis Advance Access published online on June 25, 2008
Carcinogenesis, doi:10.1093/carcin/bgn150
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Sp1 and p73 Activate PUMA Following Serum Starvation

Lihua Ming*, Tsukasa Sakaida*, Wen Yue, Anupma Jha, Lin Zhang and Jian Yu

University of Pittsburgh Cancer Institute, Departments of Pathology, and Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213

Address correspondence to: Jian Yu, Ph.D., University of Pittsburgh Cancer Institute, Hillman Cancer Center Research Pavilion, Suite 2.42h, 5117 Centre Ave., Pittsburgh, PA 15213. Fax: 412-623-7778; E-mail: yuj2{at}upmc.edu.

PUMA, p53 up-regulated modulator of apoptosis, plays an essential role in p53-dependent apoptosis following DNA damage. PUMA also mediates apoptosis independent of p53. In this study, we investigated the role and mechanism of PUMA induction in response to serum starvation in p53-deficient cancer cells. Following serum starvation, the binding of Sp1 to the PUMA promoter significantly increased, while inhibition of Sp1 completely abrogated PUMA induction. p73 was found to be upregulated by serum starvation and mediate PUMA induction through the p53 binding sites in the PUMA promoter. Sp1 and p73β appeared to cooperatively activate PUMA transcription, which is inhibited by the PI3K/AKT pathway. Furthermore, knockdown of PUMA suppressed serum starvation-induced apoptosis in leukemia cells. Our results suggest that transcription factors Sp1 and p73 mediate p53-independent induction of PUMA following serum starvation to trigger apoptosis in human cancer cells.

* These authors contribute equally to this work.

Received March 28, 2008; revised June 5, 2008; accepted June 13, 2008.


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[Abstract] [Full Text] [PDF]


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