This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Li, D. Articles by Benjamin, T. Search for Related Content PubMed PubMed Citation Articles by Li, D. Articles by Benjamin, T.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, May 2004, p. 3885-3893, Vol. 24, No. 9
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.9.3885-3893.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

p150^Sal2 Is a p53-Independent Regulator of p21^WAF1/CIP

Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115

Received 5 September 2003/ Returned for modification 26 September 2003/ Accepted 21 January 2004

p150^Sal2, a vertebrate homologue of the Drosophila melanogaster homeotic transcription factor Spalt, has previously been shown to be a binding target of the polyomavirus large T antigen. p150^Sal2 acts as an inhibitor of viral DNA synthesis, and the binding of p150^Sal2 by large T overcomes this inhibition. The present study focuses on the effects of p150^Sal2 on the growth and survival of ovarian carcinoma (OVCA) cells that are deficient in expression of p150^Sal2 and of normal established human ovarian surface epithelial (HOSE) cells which abundantly express the protein. Transient expression of exogenous p150^Sal2 in OVCA cells that show little or no endogenous expression resulted in inhibition of DNA synthesis and colony formation and in increased apoptosis. OVCA cells stably transfected and expressing physiological levels of p150^Sal2 showed reduced tumorigenicity accompanied by increased expression of p21^WAF1/CIP1 (p21) and BAX. Conversely, reduction of endogenous levels of p150^Sal2 in HOSE resulted in reduced p21 expression and increased DNA synthesis. p150^Sal2 bound to the p21 promoter adjacent to the known p53 binding sites and stimulated transcription in the absence of p53. We propose that p150^Sal2, acting in part as a p53-independent regulator of p21 and BAX, can function in some cell types as a regulator of cell growth and survival.

This article has been cited by other articles:

• Choi, B. H., Kim, C. G., Bae, Y.-S., Lim, Y., Lee, Y. H., Shin, S. Y. (2008). p21Waf1/Cip1 Expression by Curcumin in U-87MG Human Glioma Cells: Role of Early Growth Response-1 Expression. Cancer Res. 68: 1369-1377 [Abstract] [Full Text]  
• Sakaki-Yumoto, M., Kobayashi, C., Sato, A., Fujimura, S., Matsumoto, Y., Takasato, M., Kodama, T., Aburatani, H., Asashima, M., Yoshida, N., Nishinakamura, R. (2006). The murine homolog of SALL4, a causative gene in Okihiro syndrome, is essential for embryonic stem cell proliferation, and cooperates with Sall1 in anorectal, heart, brain and kidney development. Development 133: 3005-3013 [Abstract] [Full Text]  
• Humphries, M. J., Limesand, K. H., Schneider, J. C., Nakayama, K. I., Anderson, S. M., Reyland, M. E. (2006). Suppression of Apoptosis in the Protein Kinase C{delta} Null Mouse in Vivo. J. Biol. Chem. 281: 9728-9737 [Abstract] [Full Text]  
• Harvey, S. A., Logan, M. P. O. (2006). sall4 acts downstream of tbx5 and is required for pectoral fin outgrowth.. Development 133: 1165-1173 [Abstract] [Full Text]  
• Dahl, J., You, J., Benjamin, T. L. (2005). Induction and Utilization of an ATM Signaling Pathway by Polyomavirus. J. Virol. 79: 13007-13017 [Abstract] [Full Text]  
• Parrish, M., Ott, T., Lance-Jones, C., Schuetz, G., Schwaeger-Nickolenko, A., Monaghan, A. P. (2004). Loss of the Sall3 Gene Leads to Palate Deficiency, Abnormalities in Cranial Nerves, and Perinatal Lethality. Mol. Cell. Biol. 24: 7102-7112 [Abstract] [Full Text]