ArticleMolecular medicine reports2018
Mechanism of HN‑3 cell apoptosis induced by carboplatin: Combination of mitochondrial pathway associated with Ca2+ and the nucleus pathways.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Liposomal Delivery of Pyronaridine as a Repurposed Inhibitor of ERCC1/XPF for the Sensitization of Colorectal Cancer Cells to Platinum Chemotherapeutics.Molecular pharmaceutics · 2026Article
- Nano-delivery of a novel inhibitor of ERCC1-XPF for targeted sensitization of colorectal cancer to platinum-based chemotherapeutics.Drug delivery and translational research · 2025Article
- Immediate postoperative effects of cytoreductive surgery with hyperthermic intraperitoneal chemotherapy using carboplatin on peritoneal tissue inflammatory and ischemic responses: an explorative porcine study.Pleura and peritoneum · 2025Article
- Exposure to select PFAS and PFAS mixtures alters response to platinum-based chemotherapy in endometrial cancer cell lines.Environmental health : a global access science source · 2023Article
- Revisiting the Anti-Cancer Toxicity of Clinically Approved Platinating Derivatives.International journal of molecular sciences · 2022Review
- Select Per- and Polyfluoroalkyl Substances (PFAS) Induce Resistance to Carboplatin in Ovarian Cancer Cell Lines.International journal of molecular sciences · 2022Article
- Failure to Guard: Mitochondrial Protein Quality Control in Cancer.International journal of molecular sciences · 2021Review
- Metallodrugs are unique: opportunities and challenges of discovery and development.Chemical science · 2020Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Laryngeal carcinomas have been recognized as a serious health threat worldwide. In the present study, the mechanism of apoptosis in HN‑3 cells induced by carboplatin (CBCDA), a widely used anti‑cancer drug, was investigated. The pro‑apoptotic effect of CBCDA in HN‑3 cells was demonstrated to be time‑ and dose‑dependent. Therefore, the stages of apoptosis were investigated in chronological order. The results demonstrated that excessive generation of cytosolic Ca2+ in HN‑3 cells was initially triggered when cells were exposed to CBCDA, followed by the appearance of mitochondrial depolarization and oxidative stress, leading to the release of apoptosis‑inducing factor. At later stages, expression of caspase‑8 was increased due to the apoptotic signals originating from CBCDA‑induced DNA damage, as well as caspase‑9 and poly ADP ribose polymerase (PARP) expression upregulation. Glutathione decreased the available CBDCA concentration, decreased apoptosis and alleviating oxidative stress, thus reducing the actual effective concentration. Mechanistic research may benefit the rational design of more efficient therapeutic strategies as well as development of novel platinum‑based agents.
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