Regulation of p53 by Hypoxia: Dissociation of Transcriptional Repression and Apoptosis from p53-Dependent Transactivation

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Published inMolecular and Cellular Biology Vol. 21; no. 4; pp. 1297 - 1310
Main Authors Koumenis, Constantinos, Alarcon, Rodolfo, Hammond, Ester, Sutphin, Patrick, Hoffman, William, Murphy, Maureen, Derr, Jennifer, Taya, Yoichi, Lowe, Scott W., Kastan, Michael, Giaccia, Amato
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.02.2001
Taylor & Francis
Subjects
Acetylation
Apoptosis - genetics
Apoptosis - physiology
Binding Sites
Cell Growth and Development
Cell Hypoxia - genetics
Cell Hypoxia - physiology
Cell Line
Cell Nucleus - metabolism
Cell Transformation, Neoplastic
DNA Damage
Genes, p53
Histone Deacetylase Inhibitors
Histone Deacetylases - metabolism
Humans
Models, Biological
Nuclear Proteins
Phosphorylation
Proto-Oncogene Proteins - genetics
Proto-Oncogene Proteins - metabolism
Proto-Oncogene Proteins c-mdm2
RNA, Messenger - genetics
RNA, Messenger - metabolism
Signal Transduction
Transcriptional Activation
Tumor Suppressor Protein p53 - chemistry
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
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Abstract Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to MCB .asm.org, visit: MCB       
AbstractList Hypoxic stress, like DNA damage, induces p53 protein accumulation and p53-dependent apoptosis in oncogenically transformed cells. Unlike DNA damage, hypoxia does not induce p53-dependent cell cycle arrest, suggesting that p53 activity is differentially regulated by these two stresses. Here we report that hypoxia induces p53 protein accumulation, but in contrast to DNA damage, hypoxia fails to induce endogenous downstream p53 effector mRNAs and proteins. Hypoxia does not inhibit the induction of p53 target genes by ionizing radiation, indicating that p53-dependent transactivation requires a DNA damage-inducible signal that is lacking under hypoxic treatment alone. At the molecular level, DNA damage induces the interaction of p53 with the transcriptional activator p300 as well as with the transcriptional corepressor mSin3A. In contrast, hypoxia primarily induces an interaction of p53 with mSin3A, but not with p300. Pretreatment of cells with an inhibitor of histone deacetylases that relieves transcriptional repression resulted in a significant reduction of p53-dependent transrepression and hypoxia-induced apoptosis. These results led us to propose a model in which different cellular pools of p53 can modulate transcriptional activity through interactions with transcriptional coactivators or corepressors. Genotoxic stress induces both kinds of interactions, whereas stresses that lack a DNA damage component as exemplified by hypoxia primarily induce interaction with corepressors. However, inhibition of either type of interaction can result in diminished apoptotic activity.
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to MCB .asm.org, visit: MCB       
Author Amato Giaccia
Constantinos Koumenis
Scott W. Lowe
William Hoffman
Rodolfo Alarcon
Jennifer Derr
Maureen Murphy
Yoichi Taya
Michael Kastan
Patrick Sutphin
Ester Hammond
AuthorAffiliation Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305 1 ; Department of Pharmacology, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111 2 ; National Cancer Center Research Institute, Chuo-ku, Tokyo 104, Japan 3 ; Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 117241 4 ; and Department of Hematology-Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee 08105 5
AuthorAffiliation_xml – name: Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305 1 ; Department of Pharmacology, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111 2 ; National Cancer Center Research Institute, Chuo-ku, Tokyo 104, Japan 3 ; Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 117241 4 ; and Department of Hematology-Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee 08105 5
Author_xml – sequence: 1
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  fullname: Koumenis, Constantinos
  organization: Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine
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  fullname: Alarcon, Rodolfo
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  surname: Hammond
  fullname: Hammond, Ester
  organization: Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine
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  givenname: Patrick
  surname: Sutphin
  fullname: Sutphin, Patrick
  organization: Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine
– sequence: 5
  givenname: William
  surname: Hoffman
  fullname: Hoffman, William
  organization: Department of Pharmacology, Fox Chase Cancer Center
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  surname: Murphy
  fullname: Murphy, Maureen
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– sequence: 7
  givenname: Jennifer
  surname: Derr
  fullname: Derr, Jennifer
  organization: Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine
– sequence: 8
  givenname: Yoichi
  surname: Taya
  fullname: Taya, Yoichi
  organization: National Cancer Center Research Institute
– sequence: 9
  givenname: Scott W.
  surname: Lowe
  fullname: Lowe, Scott W.
  organization: Cold Spring Harbor Laboratory, Cold Spring Harbor
– sequence: 10
  givenname: Michael
  surname: Kastan
  fullname: Kastan, Michael
  organization: Department of Hematology-Oncology, St. Jude Children's Research Hospital
– sequence: 11
  givenname: Amato
  surname: Giaccia
  fullname: Giaccia, Amato
  email: giaccia@stanford.edu
  organization: Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine
BackLink https://www.ncbi.nlm.nih.gov/pubmed/11158315$$D View this record in MEDLINE/PubMed
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Present address: Department of Radiation Oncology, Wake Forest University School of Medicine, Winston-Salem, NC 27157.
Corresponding author. Mailing address: Stanford University School of Medicine, CCSR-South, Room 1255, 269 Campus Drive, Stanford, CA 94305-5152. Phone: (650) 723-7366. Fax: (650) 723-7382. E-mail: giaccia@stanford.edu.
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Snippet Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley...
Hypoxic stress, like DNA damage, induces p53 protein accumulation and p53-dependent apoptosis in oncogenically transformed cells. Unlike DNA damage, hypoxia...
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SubjectTerms Acetylation
Apoptosis - genetics
Apoptosis - physiology
Binding Sites
Cell Growth and Development
Cell Hypoxia - genetics
Cell Hypoxia - physiology
Cell Line
Cell Nucleus - metabolism
Cell Transformation, Neoplastic
DNA Damage
Genes, p53
Histone Deacetylase Inhibitors
Histone Deacetylases - metabolism
Humans
Models, Biological
Nuclear Proteins
Phosphorylation
Proto-Oncogene Proteins - genetics
Proto-Oncogene Proteins - metabolism
Proto-Oncogene Proteins c-mdm2
RNA, Messenger - genetics
RNA, Messenger - metabolism
Signal Transduction
Transcriptional Activation
Tumor Suppressor Protein p53 - chemistry
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
Title Regulation of p53 by Hypoxia: Dissociation of Transcriptional Repression and Apoptosis from p53-Dependent Transactivation
URI http://mcb.asm.org/content/21/4/1297.abstract
https://www.tandfonline.com/doi/abs/10.1128/MCB.21.4.1297-1310.2001
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