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Cited by 57Cancer-related Molecular PathwaysCell death mechanisms and regulationHeat shock proteins research

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Selective induction of apoptosis in mutant p53 premalignant and malignant cancer cells by PRIMA-1 through the c-Jun-NH2-kinase pathway

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Li, Yin, Mao, Yuehua, Brandt-Rauf, Paul W., Williams, Ann C., Fine, Robert L.·2005·Molecular Cancer Therapeutics
DOI 10.1158/1535-7163.mct-04-0206
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Abstract

PRIMA-1 (p53 reactivation and induction of massive apoptosis) is a chemical compound that was originally identified as a selective mutant p53-dependent growth suppressor by screening a library of low-molecular-weight compounds. However, its mechanism of action is unknown. In this study, we examined toxicity of PRIMA-1 to three premalignant human colorectal adenoma cell lines (RG/C2, BR/C1, and AA/C1) and four colorectal carcinoma cell lines (DLD-1, SW480, LOVO, and HCT116) and its mechanism of action. It selectively induced apoptosis only in the mutant p53 premalignant and malignant colon cell lines, but was not toxic to the wild-type p53 premalignant and malignant colon cell lines. Using stable transfectants of temperature-sensitive p53 mutant Ala(143) in null p53 H1299 lung cancer cells, we found that PRIMA-1 induced significantly more apoptosis in cells with mutant p53 conformation (37 degrees C) than the wild-type p53 conformation (32.5 degrees C). Cell cycle analysis indicated that its inhibition of cell growth was correlated with induction of G(2) arrest. Western blot analysis showed PRIMA-1 increased p21 and GADD45 expression selectively in the mutant p53 cells. However, Fas, Bcl-2 family proteins, and caspases were not involved in PRIMA-1-induced cell death. The c-Jun-NH(2)-kinase (JNK) inhibitor SP 600125, but not p38 mitogen-activated protein kinase inhibitor SB 203580 or extracellular signal-regulated kinase inhibitor PD 98059, blocked PRIMA-1-induced apoptosis. Transfection with a dominant-negative phosphorylation mutant JNK, but not a dominant-negative p38 or wild-type JNK, inhibited PRIMA-1-induced cell death, suggesting that the JNK pathway plays an important role in PRIMA-1-induced apoptosis. PRIMA-1 is a highly selective small molecule toxic to p53 mutant cells and may serve as a prototype for the development of new p53-targeting agents for therapy of premalignant and malignant cells.

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Metadata

Authors
Li, Y., Mao, Y., Brandt-Rauf, P. W., Williams, A. C., & Fine, R. L.
Affiliations
  • Columbia University Irving Medical Center (US)
  • Columbia University (US)
  • 2Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University Medical Center, New York, New York and
  • University of Bristol (GB)
ORCID
Williams, Ann C.
Venue
Molecular Cancer Therapeutics
Publisher
American Association for Cancer Research (AACR)
Published
2005-06-01
Volume
4
Issue
6
Pages
901-909
ISSN
  • 1535-7163 (ISSN-L)
  • 1538-8514
DOI
10.1158/1535-7163.mct-04-0206
OpenAlex
W1980630771
Cited by
57
References
3
Citations by year
2023: 1 · 2022: 1 · 2021: 3 · 2020: 2 · 2019: 1 · 2018: 2 · 2017: 1 · 2015: 2 · 2014: 4 · 2013: 5 · 2012: 3
FWCI
3.11
Type
journal article
Language
en
Open access
Locations
  • Molecular Cancer Therapeutics (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • University of Bristol
  • Karolinska Institutet
  • National Institutes of Health
  • National Cancer Institute (R01CA082528, R01-CA 82528)
  • National Institute for Occupational Safety and Health (R01-OH07590)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
Keywords
PRIMA-1, mutant p53, apoptosis, c-Jun NH2-kinase, colorectal cancer, colorectal adenoma, JNK signaling, G2 cell cycle arrest, p21, GADD45, temperature-sensitive p53, selective cytotoxicity
MeSH terms
Aza Compounds, Cell Line, Cell Transformation, Neoplastic, Colonic Neoplasms, Humans, Lung Neoplasms, Neoplasms, Precancerous Conditions, RNA, Messenger, Temperature, Signal Transduction, Tumor Suppressor Protein p53, Apoptosis, Bridged Bicyclo Compounds, Heterocyclic, Protein Kinase Inhibitors, JNK Mitogen-Activated Protein Kinases

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