Cited by 267Cancer-related Molecular PathwaysCell death mechanisms and regulationPI3K/AKT/mTOR signaling in cancer

Growth arrest induced by wild-type p53 protein blocks cells prior to or near the restriction point in late G1 phase.

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Lin, D, Shields, M T, Ullrich, S J, Appella, E, Mercer, W E·1992·Proceedings of the National Academy of Sciences

Abstract

Conditional expression of wild-type (wt) p53 protein in a glioblastoma tumor cell line has been shown to be growth inhibitory. We have now more precisely localized the position in the cell cycle where growth arrest occurs. We show that growth arrest occurs prior to or near the restriction point in late G1 phase of the cell cycle. The effect of wt p53 protein on the expression of four immediate-early genes (c-FOS, c-JUN, JUN-B, and c-MYC), one delayed-early gene (ornithine decarboxylase), and two late-G1/S-phase genes (B-MYB and DNA polymerase alpha) was also examined. Of this subset of growth response genes, only the expression of B-MYB and DNA polymerase alpha was significantly repressed. The possibility that decreased expression of B-MYB may be an important component of growth arrest mediated by wt p53 protein is discussed.

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Crossref · 10.1073/pnas.89.19.9210

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Authors
Lin, D., Shields, M. T., Ullrich, S. J., Appella, E., & Mercer, W. E.
Affiliations
Thomas Jefferson University (US)
Venue
Proceedings of the National Academy of Sciences
Published
1992-10
Volume
89
Issue
19
Pages
9210-9214
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W1971928705
Cited by
267
References
40
Citations by year
2025: 1 · 2023: 2 · 2021: 2 · 2020: 2 · 2018: 1 · 2017: 3 · 2014: 2 · 2013: 1 · 2012: 4
FWCI
14.10
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ca042866-03, 1t32ca009644-01a1)
  • National Cancer Institute (CA42866, CA09644)
  • National Center for Research Resources (SO 7RR05417)
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 › PI3K/AKT/mTOR signaling in cancer
Keywords
wild-type p53, growth arrest, restriction point, cell cycle, glioblastoma, B-Myb, DNA polymerase alpha, c-fos, c-Jun, JunB, c-Myc, ornithine decarboxylase, immediate early genes, delayed-early genes, gene expression inhibition
MeSH terms
Cell Cycle, Cell Division, Cycloheximide, Dexamethasone, DNA Polymerase II, Glioma, Humans, Ornithine Decarboxylase, RNA, Messenger, RNA, Neoplasm, Tumor Cells, Cultured, Blotting, Northern, Tumor Suppressor Protein p53, G1 Phase, Genes, myc, Genes, jun, Genes, fos

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