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Induction of p53-mediated apoptosis and recovery of chemosensitivity through p53 transduction in human glioblastoma cells by cisplatin
Open accessAbstract
Cisplatin is a DNA-damaging chemotherapeutic drug that may have a role in the adjuvant chemotherapy of several solid tumors, such as malignant glioblastoma, and the status of p53 tumor suppressor protein is a critical determinant of cisplatin chemosensitivity. In the present study, we showed the relationship of p53 status and chemosensitivity of cisplatin between two human malignant glioblastoma cell lines, A172 and T98G, harboring wild-type and mutant-type p53, respectively. Cisplatin was found to be more cytotoxic to A172 than T98G cells in a time- and concentration-dependent manner. Cisplatin-induced cytotoxicity manifested as apoptosis, characterized by genomic DNA fragmentation, nuclear condensation and an increase in sub-G1 population. Cisplatin induced the accumulation of p53 and p21 proteins in A172 cells, but not in T98G cells. The introduction of the adenovirus-mediated wild-type p53 gene into T98G cells resulted in the decrease of viability as well as the increase in sub-G1 population with p53 accumulation, activation of caspase-3 protease and release of cytochrome c from the mitochondria. These data strongly suggest that the expression of p53 is essential for the cytotoxic effect of cisplatin in human malignant glioblastoma cells, A172 and T98G, and the introduction of apoptotic signal molecules, such as p53, will be beneficial to achieve chemosensitivity in malignant glioma.
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“p53 inactivation is correlated with a more invasive [30], less apoptotic [31], more proliferative [27], and more stem-like [28] phenotype.”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [31]
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“GBM cell lines possessing inactivated mutant p53 (mut-p53) are more resistant to DNA-damaging therapeutic drugs, such as cisplatin [31].”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [31]
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- Mazzatti DJ, Lee YJ, Helt CE, O'Reilly MA and Keng PC: p53 modulates radiation sensitivity independent of p21 transcriptional activation. Am J Clin Oncol 28: 43-50, 2005.
Cited by
Florea, A.-M., & Büsselberg, D. (2011) · Cancers · doi:10.3390/cancers3011351 · Cited by 1,759
Epidemiology of Glioblastoma Multiforme–Literature Review
Grochans, S., Cybulska, A. M., Simińska, D., Korbecki, J., Kojder, K., Chlubek, D., & Baranowska-Bosiacka, I. (2022) · Cancers · doi:10.3390/cancers14102412 · Cited by 630
The p53 Pathway in Glioblastoma
Zhang, Y., Dube, C., Gibert, M., Cruickshanks, N., Wang, B., Coughlan, M., Yang, Y., Setiady, I., Deveau, C., Saoud, K., et al. (2018) · Cancers · doi:10.3390/cancers10090297 · Cited by 440
Rocha, C. R. R., Garcia, C. C. M., Vieira, D. B., Quinet, A., de Andrade-Lima, L. C., Munford, V, Belizário, J. E., & Menck, C. F. M. (2014) · Cell Death & Disease · doi:10.1038/cddis.2014.465 · Cited by 164
Lulla, R. R., Goldman, S., Yamada, T., Beattie, C. W., Bressler, L. R., Pacini, M., Pollack, I. F., Fisher, P. G., Packer, R. J., Dunkel, I. J., et al. (2016) · Neuro-Oncology · doi:10.1093/neuonc/now047 · Cited by 152
Metadata
- Authors
- Park, C.-M., Park, M.-J., Kwak, H.-J., Moon, S.-I., Yoo, D.-H., Lee, H.-C., Park, I.-C., Rhee, C. H., & Hong, S.-I.
- Affiliations
- Korea Institute of Radiological and Medical Sciences (KR)
- Venue
- International Journal of Oncology
- Publisher
- Spandidos Publications
- Published
- 2006-01-01
- Volume
- 28
- Issue
- 1
- Pages
- 119-25
- ISSN
- 1019-6439 (ISSN-L)
- 1791-2423
- OpenAlex
- W1996719655
- Cited by
- 58
- References
- 0
- Citations by year
- 2025: 2 · 2024: 5 · 2023: 4 · 2022: 3 · 2021: 2 · 2020: 6 · 2019: 3 · 2018: 4 · 2017: 3 · 2016: 2 · 2015: 2 · 2014: 3 · 2013: 4 · 2012: 5
- FWCI
- 1.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- International Journal of Oncology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Oncology › Glioma Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- p53, cisplatin, glioblastoma, apoptosis, chemosensitivity, wild-type p53, mutant p53, p21, caspase-3, cytochrome c release, DNA fragmentation, A172 cells, T98G cells
- MeSH terms
- Brain Neoplasms, Cisplatin, DNA Damage, Enzyme Activation, Glioblastoma, Humans, Transduction, Genetic, Tumor Cells, Cultured, Genes, p53, Tumor Suppressor Protein p53, Apoptosis, Caspases, Cytochromes c, Caspase 3, Caspase 9
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- The paper
- Park, C.-M., Park, M.-J., Kwak, H.-J., Moon, S.-I., Yoo, D.-H., Lee, H.-C., Park, I.-C., Rhee, C. H., & Hong, S.-I. (2006). Induction of p53-mediated apoptosis and recovery of chemosensitivity through p53 transduction in human glioblastoma cells by cisplatin. International Journal of Oncology. https://doi.org/10.3892/ijo.28.1.119
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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.
