Skip Navigation



Carcinogenesis Advance Access published online on March 28, 2003
Carcinogenesis, doi:10.1093/carcin/bgg044
© 2003 by Oxford University Press
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
24/7/1177    most recent
bgg044v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Renton, A.
Right arrow Articles by Lu, X.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Renton, A.
Right arrow Articles by Lu, X.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2003 Oxford University Press

CANCER BIOLOGY

Hypoxia induces p53 through a pathway distinct from most DNA damaging and stress-inducing agents

Alan Renton 1, Susana Llanos 1, Xin Lu 1*

1 Ludwig Institute for Cancer Research, Imperial College of Science, Technology and Medicine at St. Mary's Campus. Norfolk Place, London, W2 1PG. U.K.

* Corresponding author. E-mail: x.lu{at}ic.ac.uk.

Received 17 June 2002 ; revised 23 December 2003 ; accepted 3 March 2003

Abstract

The p53 tumour suppressor gene is a transcription factor that can induce cell cycle arrest and apoptosis. In response to various stress-inducing signals, p53 level increases and this accompanied with increased activities of p53. Interestingly, the methylxanthine caffeine can abrogate the p53 accumulation induced by certain DNA-damaging agents by an unknown mechanism. In an effort to understand how different signals induce p53, human tumour cell lines were treated with combinations of various stress-inducing agents and caffeine. Caffeine inhibited the accumulation of p53 induced by Leptomycin B (LMB), an inhibitor of CRM1, but not ALLN, a proteasome inhibitor. Furthermore, caffeine also inhibited the accumulation of p53 by a variety of stress-inducing agents in vivo, such as 5-fluorouracil, doxorubicin, mitomycin C, camptothecin, and roscovitine. However, caffeine failed to affect the accumulation of p53 in hypoxia-treated cells. These results suggested that hypoxia must use a distinct pathway from most DNA damaging and stress inducing agents to induce p53.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Neurosci.Home page
R. Helton, J. Cui, J. R. Scheel, J. A. Ellison, C. Ames, C. Gibson, B. Blouw, L. Ouyang, I. Dragatsis, S. Zeitlin, et al.
Brain-Specific Knock-Out of Hypoxia-Inducible Factor-1{alpha} Reduces Rather Than Increases Hypoxic-Ischemic Damage
J. Neurosci., April 20, 2005; 25(16): 4099 - 4107.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
G.-i. Kusakai, A. Suzuki, T. Ogura, S.'i. Miyamoto, A. Ochiai, M. Kaminishi, and H. Esumi
ARK5 Expression in Colorectal Cancer and Its Implications for Tumor Progression
Am. J. Pathol., March 1, 2004; 164(3): 987 - 995.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
K. A. Seta and D. E. Millhorn
Functional genomics approach to hypoxia signaling
J Appl Physiol, February 1, 2004; 96(2): 765 - 773.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.