The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Mutant p53 mediates survival of breast cancer cells
Open accessAbstract
BACKGROUND: p53 is the most commonly mutated tumour-suppressor gene in human cancers. Unlike other tumour-suppressor genes, most p53 cancer mutations are missense mutations within the core domain, leading to the expression of a full-length mutant p53 protein. Accumulating evidence has indicated that p53 cancer mutants not only lose tumour suppression activity but also gain new oncogenic activities to promote tumourigenesis. METHODS: The endogenous mutant p53 function in human breast cancer cells was studied using RNA interference (RNAi). Gene knockdown was confirmed by quantitative PCR and western blotting. Apoptosis was evaluated by morphological changes of cells, their PARP cleavage and annexin V staining. RESULTS: We show that cancer-associated p53 missense mutants are required for the survival of breast cancer cells. Inhibition of endogenous mutant p53 by RNAi led to massive apoptosis in two mutant p53-expressing cell lines, T47D and MDA-MB-468, but not in the wild-type p53-expressing cells, MCF-7 and MCF-10A. Reconstitution of an RNAi-insensitive mutant p53 in MDA-MB-468 cells completely abolished the apoptotic effects after silencing of endogenous mutant p53, suggesting the specific survival effects of mutant p53. The apoptotic effect induced by mutant p53 ablation, however, is independent of p63 or p73 function. CONCLUSION: These findings provide clear evidence of a pro-survival 'gain-of-function' property of a subset of p53 cancer mutants in breast cancer cells.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607 · cited 1×
“…is the most extensively studied tumour-suppressor gene, encoding a sequence-specific transcriptional regulator that controls a plethora of biological functions, including cell-cycle progression, senescence, differentiation, DNA repair, and apoptosis (Vogelstein et al, 2000; Oren, 2001, 2003).”
Blinded by the Light: The Growing Complexity of p53
Vousden, K. H., & Prives, C. (2009) · Cell · doi:10.1016/j.cell.2009.04.037 · Cited by 3,163
Hypoxia-mediated selection of cells with diminished apoptotic potential in solid tumours
Graeber, T. G., Osmanian, C., Jacks, T., Housman, D. E., Koch, C. J., Lowe, S. W., & Giaccia, A. J. (1996) · Nature · doi:10.1038/379088a0 · Cited by 2,300
Noxa, a BH3-Only Member of the Bcl-2 Family and Candidate Mediator of p53-Induced Apoptosis
Oda, E., Ohki, R., Murasawa, H., Nemoto, J., Shibue, T., Yamashita, T., Tokino, T., Taniguchi, T., & Tanaka, †. N. (2000) · Science · doi:10.1126/science.288.5468.1053 · Cited by 2,112
Mutant p53 gain of function in two mouse models of Li-Fraumeni syndrome
Olive, K. P., Tuveson, D. A., Ruhe, Z. C., Yin, B., Willis, N. A., Bronson, R. T., Crowley, D., & Jacks, T. (2004) · Cell · doi:10.1016/j.cell.2004.11.004 · Cited by 1,308
Di Agostino, S., Strano, S., Emiliozzi, V., Zerbini, V., Mottolese, M., Sacchi, A., Blandino, G., & Piaggio, G. (2006) · Cancer Cell · doi:10.1016/j.ccr.2006.08.013 · Cited by 418
Birch, J. M., Blair, V., Kelsey, A. M., Evans, D. G., Harris, M., Tricker, K. J., & Varley, J. M. (1998) · Oncogene · doi:10.1038/sj.onc.1202033 · Cited by 200
Zalcenstein, A., Stambolsky, P., Weisz, L., Müller, M., Wallach, D., Goncharov, T. M., Krammer, P. H., Rotter, V., & Oren, M. (2003) · Oncogene · doi:10.1038/sj.onc.1206724 · Cited by 123
Cited by
Mutant p53 in Cancer: New Functions and Therapeutic Opportunities
Muller, P. A. J., & Vousden, K. H. (2014) · Cancer Cell · doi:10.1016/j.ccr.2014.01.021 · Cited by 1,545
Gain-of-function p53 mutants co-opt chromatin pathways to drive cancer growth
Zhu, J., Sammons, M. A., Donahue, G., Dou, Z., Vedadi, M., Getlik, M., Barsyte-Lovejoy, D., Al-awar, R., Katona, B. W., Shilatifard, A., et al. (2015) · Nature · doi:10.1038/nature15251 · Cited by 493
Mirzayans, R., Andrais, B., Scott, A., & Murray, D. (2012) · Journal of Biomedicine and Biotechnology · doi:10.1155/2012/170325 · Cited by 257
Acetylation regulates ribonucleotide reductase activity and cancer cell growth
Chen, G., Luo, Y., Warncke, K., Sun, Y., Yu, D. S., Fu, H., Behera, M., Ramalingam, S. S., Doetsch, P. W., Duong, D. M., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-11214-9 · Cited by 82
YI, B.-R., CHOI, K. J., KIM, S. U., & CHOI, K.-C. (2012) · International Journal of Oncology · doi:10.3892/ijo.2012.1523 · Cited by 32
Metadata
- Authors
- Lim, L. Y., Vidnovic, N., Ellisen, L. W., & Leong, C.-O.
- Venue
- British Journal of Cancer
- Published
- 2009-09-22
- Volume
- 101
- Issue
- 9
- Pages
- 1606-1612
- ISSN
- 0007-0920 (ISSN-L)
- 1532-1827
- OpenAlex
- W2060798006
- Cited by
- 175
- References
- 8
- FWCI
- 3.28
- Type
- journal article
- Language
- en
- Open access
- hybrid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Mutant p53 mediates survival of breast cancer cells. https://app.cochat.ai/papers/10.1038/sj.bjc.6605335
- The paper
- Lim, L. Y., Vidnovic, N., Ellisen, L. W., & Leong, C.-O. (2009). Mutant p53 mediates survival of breast cancer cells. British Journal of Cancer. https://doi.org/10.1038/sj.bjc.6605335
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
