The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
Mdm2 sensitizes MCF7 breast cancer cells to cisplatin or carboplatin
Abstract
Overexpression of Mdm2 in cancer cells with otherwise wild-type p53 is believed to be an alternative mechanism for p53 inactivation during carcinogenesis. Because a number of genetic alterations that inactivate p53, including mutation, homozygous deletion, or viral oncoprotein expression (e.g. HPV16-E6), inhibit DNA repair, we tested the hypothesis that Mdm2 would likewise inhibit DNA repair. Repair of cisplatin-induced DNA damage was reduced in MCF7 cells overexpressing Mdm2, compared to MCF7 cells in which wild-type p53 function was intact. MCF7-Mdm2 cells exhibited preferential sensitivity to cisplatin and carboplatin. MCF7-Mdm2 cells showed a pronounced S-phase arrest after cisplatin treatment, similar to that observed in mutant-p53 cells in the present and prior studies. MCF7 cells with intact wild-type p53, on the other hand, arrested primarily in G2/M phase after cisplatin treatment. These findings indicate that Mdm2 overexpression can recapitulate the effect of p53 mutations on DNA repair of cisplatin lesions.
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“Cell cycle analysis indicated that the TMD231 cell line had both diploid and aneuploid subpopulations and that carboplatin-treated TMD231 cells accumulated in S and G2/M in both subpopulations (Supplemental Fig. S3), which is consistent with previous reports that platinum agents lead to S and G2/M accumulation (31).”
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 [31]
Citations
Cites
Rescue of early embryonic lethality in mdm2-deficient mice by deletion of p53
de Oca Luna, R. M., Wagner, D. S., & Lozano, G. (1995) · Nature · doi:10.1038/378203a0 · Cited by 1,420 · cited 1×
“There is substantial genetic evidence that Mdm2 may downregulate p53 activity in normal cells even in the absence of exogenous DNA damage [ 29 , 30].”
Backgroundp21 is necessary for the p53-mediated G1 arrest in human cancer cells.
Waldman, T. A., Kinzler, K. W., & Vogelstein, B. (1995) · PubMed · Cited by 1,188
The MDM2 gene amplification database
Momand, J. (1998) · Nucleic Acids Research · doi:10.1093/nar/26.15.3453 · Cited by 982
Hwang, B. J., Ford, J. M., Hanawalt, P. C., & Chu, G. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.2.424 · Cited by 581
p53 modulation of TFIIH–associated nucleotide excision repair activity
Wang, X. W., Yeh, H., Schaeffer, L., Roy, R., Moncollin, V., Egly, J., Wang, Z., Friedberg, E. C., Evans, M. K., Taffe, B. G., et al. (1995) · Nature Genetics · doi:10.1038/ng0695-188 · Cited by 555
Disruption of p53 function sensitizes breast cancer MCF-7 cells to cisplatin and pentoxifylline.
Fan, S., Smith, M. L., Rivet, D. J., Duba, D. E., Zhan, Q., Kohn, K. W., Fornace, A. J., & O'Connor, P. M. (1995) · PubMed · Cited by 490
Self-citationUCN-01: a potent abrogator of G2 checkpoint function in cancer cells with disrupted p53
Wang, Q., Fan, S., Eastman, A., Worland, P. J., Sausville, E. A., & O'Connor, P. M. (1996) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/88.14.956 · Cited by 453
Involvement of the p53 tumor suppressor in repair of u.v.-type DNA damage.
Smith, M. L., Chen, I. T., Zhan, Q., O'Connor, P. M., & Fornace, A. J. (1995) · PubMed · Cited by 364
Self-citationFord, J. M., & Hanawalt, P. C. (1997) · Journal of Biological Chemistry · doi:10.1074/jbc.272.44.28073 · Cited by 357
Ford, J. M., & Hanawalt, P. C. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.19.8876 · Cited by 343
Research works printed but not linked: 4
- Smith ML, Chen IT, Zhan Q, O'Connor PM, Fornace AJ, Jr: Involvement of the p53 suppressor in repair of UV-type DNA damage. Oncogene 10: 1053–1059, 1995
- Freedman DA, Levine AJ: Regulation of the p53 protein by Mdm2 oncoprotein. Cancer Res 59: 1–7, 1999
- Smith ML, Hollander MC, Bortnick RA, Fornace AJ, Jr: Measurements of DNA repair synthesis in mouse embryo fibroblasts lacking p53, gadd45, cip1(wafl) or gadd45 and cip1 genes. Proc Am Assoc Cancer Res 39: 279, 1998
- Ford JM, Smith ML, Hanawalt PC, Fornace AJ, Jr: Involvement of p53–responsive genes in murine nucleotide excision DNA repair. Proc Am Assoc Cancer Res 40: 101, 1999
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Ahmad, S. (2010) · Chemistry & Biodiversity · doi:10.1002/cbdv.200800340 · Cited by 222
Hershberger, P. A., McGuire, T. F., Yu, W., Zuhowski, E. G., Schellens, J. H. M., Egorin, M. J., Trump, D. L., & Johnson, C. S. (2002) · PubMed · Cited by 85
Muscella, A., Calabriso, N., Fanizzi, F. P., Pascali, S. A. D., Urso, L., Ciccarese, A., Migoni, D., & Marsigliante, S. (2007) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0707576 · Cited by 73
Muscella, A., Calabriso, N., Fanizzi, F. P., Pascali, S. A. D., Urso, L., Ciccarese, A., Migoni, D., & Marsigliante, S. (2008) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0707646 · Cited by 61
Tonsing-Carter, E., Bailey, B. J., Saadatzadeh, M. R., Ding, J., Wang, H., Sinn, A. L., Peterman, K. M., Spragins, T. K., Silver, J. M., Sprouse, A. A., et al. (2015) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-15-0237 · Cited by 42
Metadata
- Authors
- Smith, M. L.
- Affiliations
- Indiana University Melvin and Bren Simon Comprehensive Cancer Center (US)
- Corresponding author
- Smith, Martin L.
- Venue
- Breast Cancer Research and Treatment
- Published
- 1999-11
- Volume
- 58
- Issue
- 2
- Pages
- 99-105
- ISSN
- 0167-6806 (ISSN-L)
- 1573-7217
- OpenAlex
- W1970749160
- Cited by
- 9
- References
- 35
- Citations by year
- 2021: 1 · 2015: 1 · 2014: 1 · 2013: 1
- FWCI
- 0.14
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Breast Cancer Research and Treatment (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
- Keywords
- MDM2, p53 inactivation, cisplatin, carboplatin, DNA repair, MCF-7 cells, breast cancer, S phase arrest, G2/M cell cycle arrest, chemosensitization, platinum-induced DNA damage
- MeSH terms
- Antineoplastic Agents, Breast Neoplasms, Cell Cycle, Cisplatin, DNA Damage, DNA Repair, Female, Flow Cytometry, Humans, Nuclear Proteins, Proto-Oncogene Proteins, Transfection, Tumor Cells, Cultured, Tumor Suppressor Protein p53, Carboplatin, Proto-Oncogene Proteins c-mdm2
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