The DOI matches its Crossref record; 70 of the 70 references it cites were found in a registry or an index.
Mechanism of Cisplatin-Induced Cytotoxicity Is Correlated to Impaired Metabolism Due to Mitochondrial ROS Generation
Open accessAbstract
The chemotherapeutic use of cisplatin is limited by its severe side effects. In this study, by conducting different omics data analyses, we demonstrated that cisplatin induces cell death in a proximal tubular cell line by suppressing glycolysis- and tricarboxylic acid (TCA)/mitochondria-related genes. Furthermore, analysis of the urine from cisplatin-treated rats revealed the lower expression levels of enzymes involved in glycolysis, TCA cycle, and genes related to mitochondrial stability and confirmed the cisplatin-related metabolic abnormalities. Additionally, an increase in the level of p53, which directly inhibits glycolysis, has been observed. Inhibition of p53 restored glycolysis and significantly reduced the rate of cell death at 24 h and 48 h due to p53 inhibition. The foremost reason of cisplatin-related cytotoxicity has been correlated to the generation of mitochondrial reactive oxygen species (ROS) that influence multiple pathways. Abnormalities in these pathways resulted in the collapse of mitochondrial energy production, which in turn sensitized the cells to death. The quenching of ROS led to the amelioration of the affected pathways. Considering these observations, it can be concluded that there is a significant correlation between cisplatin and metabolic dysfunctions involving mROS as the major player.
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Cites
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Cited by
ROS and the DNA damage response in cancer
Srinivas, U. S., Tan, B. W. Q., Vellayappan, B. A., & Jeyasekharan, A. D. (2019) · Redox Biology · doi:10.1016/j.redox.2018.101084 · Cited by 2,144
Advances in Our Understanding of the Molecular Mechanisms of Action of Cisplatin in Cancer Therapy
Tchounwou, P. B., Dasari, S., Noubissi, F. K., Ray, P., & Kumar, S. (2021) · Journal of Experimental Pharmacology · doi:10.2147/jep.s267383 · Cited by 384
ROS as a novel indicator to predict anticancer drug efficacy
Zaidieh, T., Smith, J. R., Ball, K. E., & An, Q. (2019) · BMC Cancer · doi:10.1186/s12885-019-6438-y · Cited by 138
Lewis, J. E., Forshaw, T. E., Boothman, D. A., Furdui, C. M., & Kemp, M. L. (2021) · Cell Systems · doi:10.1016/j.cels.2020.12.001 · Cited by 61
Hoogstraten, C. A., Smeitink, J. A. M., Russel, F. G. M., & Schirris, T. J. J. (2022) · Frontiers in Toxicology · doi:10.3389/ftox.2022.842396 · Cited by 30
Metadata
- Authors
- Choi, Y.-M., Kim, H.-K., Shim, W., Anwar, M. A., Kwon, J.-W., Kwon, H.-K., Kim, H. J., Jeong, H., Kim, H. M., Hwang, D., Kim, H. S., & Choi, S.
- Venue
- PLOS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2015-08-06
- Volume
- 10
- Issue
- 8
- Pages
- e0135083
- ISSN
- 1932-6203 (ISSN-L)
- OpenAlex
- W1722494167
- Cited by
- 279
- References
- 70
- FWCI
- 9.87
- Type
- journal article
- Language
- en
- Open access
- gold
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- Choi, Y.-M., Kim, H.-K., Shim, W., Anwar, M. A., Kwon, J.-W., Kwon, H.-K., Kim, H. J., Jeong, H., Kim, H. M., Hwang, D., Kim, H. S., & Choi, S. (2015). Mechanism of Cisplatin-Induced Cytotoxicity Is Correlated to Impaired Metabolism Due to Mitochondrial ROS Generation. PLOS ONE. https://doi.org/10.1371/journal.pone.0135083
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