Mutant p53 in MDA-MB-231 breast cancer cells is stabilized by elevated phospholipase D activity and contributes to survival signals generated by phospholipase D

Hui, L; Zheng, Y; Yan, Y; Bargonetti, J; Foster, D A

doi:10.1038/sj.onc.1209735

Cited by 218Cancer-related Molecular PathwaysPI3K/AKT/mTOR signaling in cancerCell death mechanisms and regulation

Mutant p53 in MDA-MB-231 breast cancer cells is stabilized by elevated phospholipase D activity and contributes to survival signals generated by phospholipase D

Hui, L, Zheng, Y, Yan, Y, Bargonetti, J, Foster, D A·2006·Oncogene

DOI 10.1038/sj.onc.1209735

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Abstract

p53 is the most commonly mutated gene in human cancer. Although the loss of tumor suppressor functions for p53 in tumorigenesis is well characterized, gain-of-function p53 mutations observed in most cancers are not as widely appreciated. The human breast cancer cell line MDA-MB-231, which has high levels of a mutant p53, has high levels of phospholipase D (PLD) activity, which provides a survival signal in these cells when deprived of serum growth factors. We report here that the mutant p53 in MDA-MB-231 cells is stabilized by the elevated PLD activity in these cells. Surprisingly, the survival of MDA-MB-231 cells deprived of serum was dependent on the mutant p53. These data indicate that a mutant p53, stabilized by elevated PLD activity, can contribute to the suppression of apoptosis in a human breast cancer cell line and suggest a rationale for the selection of p53 mutations early in tumorigenesis to suppress apoptosis in an emerging tumor.

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The mtp53 R280K mutation in MDA-MB-231 and TMD231 cells has been reported to have gain-of-function properties, though its exact role remains unclear.
“The mtp53 R280K mutation in the MDA-MB-231 and the TMD231 cells has been reported to have gain-of function properties (34); however, its exact role is still not well understood.”
From Potentiation of carboplatin-mediated DNA damage by the Mdm2 modulator Nutlin-3a in a humanized orthotopic breast-to-lung metastatic model (2015) · cites this paper as [34]

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Molecular Diagnostics
Lim, L., Vidnovic, N., Ellisen, L., & Leong, C.-O. (2009)

Authors: Hui, L., Zheng, Y., Yan, Y., Bargonetti, J., & Foster, D. A.
Affiliations: Hunter College (US)
Corresponding author: Foster, D A
ORCID: Zheng, Y
Yan, Y
Bargonetti, J
Foster, D A
Venue: Oncogene
Publisher: Springer Science and Business Media LLC
Published: 2006-06-19
Volume: 25
Issue: 55
Pages: 7305-7310
ISSN: 0950-9232 (ISSN-L)
1476-5594
DOI: 10.1038/sj.onc.1209735
OpenAlex: W2059200921
Cited by: 218
References: 37
Citations by year: 2026: 6 · 2025: 14 · 2024: 13 · 2023: 14 · 2022: 14 · 2021: 19 · 2020: 13 · 2019: 11 · 2018: 12 · 2017: 17 · 2016: 12 · 2015: 5 · 2014: 13 · 2013: 11 · 2012: 9
FWCI: 2.43
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Oncogene (publishedVersion)
PubMed (publishedVersion)
Funders: National Cancer Institute (CA 46677)
National Institute of General Medical Sciences (GM60654, S06GM060654)
National Center for Research Resources (RR-03037)
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords: mutant p53, phospholipase D, MDA-MB-231 cells, breast cancer, protein stabilization, apoptosis inhibition, cell survival signaling, serum deprivation, tumor suppressor function
MeSH terms: Breast Neoplasms, Cell Survival, Humans, Phospholipase D, Protein Kinases, Tumor Suppressor Protein p53, Mitogen-Activated Protein Kinases, Cell Line, Tumor, TOR Serine-Threonine Kinases

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Mutant p53 in MDA-MB-231 breast cancer cells is stabilized by elevated phospholipase D activity and contributes to survival signals generated by phospholipase D

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