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PMID: 7731711 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S.

p53-mediated apoptosis in HeLa cells can be overcome by excess pRB.

Oncogene ·Vol. 10 ·No. 8 ·1995-04-20 ·Pages 1563-71

Haupt Y, Rowan S, Oren M

Abstract

Studies on DNA tumor viruses have suggested a link between p53 and pRB in the control of cell growth and apoptosis. We examined the role of pRB in the control of p53-mediated apoptosis in HeLa cells, in which the activities of p53 and members of the pRB family are very low. Transient overexpression of wild type (wt) p53 in HeLa cells induced apoptotic cell death. Importantly, coexpression of functional pRB resulted in significant protection of HeLa cells from p53-mediated apoptosis, without interfering with the transcriptional activity of wt p53. These results suggest that pRB, and possibly other pRB-related proteins, play a major role in the decision of whether cells respond to activated p53 by undergoing growth arrest or apoptosis. Our findings demonstrate a direct link between these two tumor suppressors in the control of cell growth and cell death.

MeSH Terms
Apoptosis Cell Cycle DNA/metabolism HeLa Cells Humans Interleukin-6/pharmacology Proto-Oncogene Proteins/physiology Proto-Oncogene Proteins c-bcl-2 Retinoblastoma Protein/physiology Transcriptional Activation Tumor Suppressor Protein p53/physiology
Chemicals
Interleukin-6 Proto-Oncogene Proteins Proto-Oncogene Proteins c-bcl-2 Retinoblastoma Protein Tumor Suppressor Protein p53 DNA
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Haupt Y
Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel.
Rowan S
Oren M
Article Info
Journal
Oncogene
Abbr.
Oncogene
ISSN
0950-9232
Published
1995-04-20
Pages
1563-71
Language
English
Region
England
NLM ID
8711562
Subset
IM
Grants
NCI NIH HHS · R01 CA 4009 · United States
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