ArticleScientific reports2020
Mitochondrial DNA alterations may influence the cisplatin responsiveness of oral squamous cell carcinoma.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers, 2 of them syntheses that pooled it.
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Who cites it
42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.
- Mitochondrial DNA (mtDNA) as fluid biomarker in neurodegenerative disorders: A systematic review.European journal of neurology · 2025Pooled it
- Genetic Variants Associated With Response to Platinum-Based Chemotherapy in Non-Small Cell Lung Cancer Patients: A Field Synopsis and Meta-Analysis.British journal of biomedical science · 2024Pooled it
- A human patient-derived organoid biobank to model tumor heterogeneity and therapeutic vulnerability for oral squamous cell carcinoma.Cell reports. Medicine · 2026Article
- Mitochondrial-targeted therapeutics in oral squamous cell carcinoma: molecular and therapeutic implications.Frontiers in medicine · 2026Review
- Natural product-induced apoptosis in oral squamous cell carcinoma via targeting mitochondrial multifunctionality.Frontiers in oncology · 2026Review
- The significance of mitochondrial DNA changes during the onset and progression of head and neck squamous cell carcinoma.Future oncology (London, England) · 2026Review
- Cisplatin resistance in oral squamous cell carcinoma: mechanisms, reversal strategies, and emerging technologies.Frontiers in physiology · 2026Review
- Thymoquinone Overcomes Hypoxia-Induced Carboplatin Resistance Through ROS-Independent Apoptosis but Promotes Cancer Stem Cell Enrichment: Implications on Oral Cancer Adaptation and Recurrence.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Rewriting nuclear epigenetic scripts in mitochondrial diseases as a strategy for heteroplasmy control.EMBO molecular medicine · 2025Article
- Mechanisms of Cisplatin-Induced Acute Kidney Injury: The Role of NRF2 in Mitochondrial Dysfunction and Metabolic Reprogramming.Antioxidants (Basel, Switzerland) · 2025Article
- Mitochondrial epigenetic mechanisms in cancer: an updated overview.Frontiers in cell and developmental biology · 2025Review
- Mitochondrial DNA Mutations and Epigenetic Regulation in Type 2 Diabetes Mellitus Development.British journal of biomedical science · 2025Review
- Potential role of heteroplasmic mitochondrial DNA mutations in modulating the subtype-specific adaptation of oral squamous cell carcinoma to cisplatin therapy.Discover oncology · 2024Article
- Direct targeting of mitochondria by cisplatin leads to cytotoxicity in zebrafish lateral-line hair cells.iScience · 2024Article
- Defects of mitochondria-lysosomes communication induce secretion of mitochondria-derived vesicles and drive chemoresistance in ovarian cancer cells.Cell communication and signaling : CCS · 2024Article
- Mitochondrion: Main organelle in orchestrating cancer escape from chemotherapy.Cancer reports (Hoboken, N.J.) · 2024Review
- Collaboration ofFuture science OA · 2024Article
- Capsaicin exerts synergistic pro-apoptotic effects with cisplatin in TSCC through the calpain pathway via TRPV1.Journal of Cancer · 2024Article
- Optimized bisulfite sequencing analysis reveals the lack of 5-methylcytosine in mammalian mitochondrial DNA.BMC genomics · 2023Article
- Mitochondrial DNA-targeted therapy: A novel approach to combat cancer.Cell insight · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin is the first-line chemotherapeutic agent for the treatment of oral squamous cell carcinoma (OSCC). However, the intrinsic or acquired resistance against cisplatin remains a major obstacle to treatment efficacy in OSCC. Recently, mitochondrial DNA (mtDNA) alterations have been reported in a variety of cancers. However, the role of mtDNA alterations in OSCC has not been comprehensively studied. In this study, we evaluated the correlation between mtDNA alterations (mtDNA content, point mutations, large-scale deletions, and methylation status) and cisplatin sensitivity using two OSCC cell lines, namely SAS and H103, and stem cell-like tumour spheres derived from SAS. By microarray analysis, we found that the tumour spheres profited from aberrant lipid and glucose metabolism and became resistant to cisplatin. By qPCR analysis, we found that the cells with less mtDNA were less responsive to cisplatin (H103 and the tumour spheres). Based on the findings, we theorised that the metabolic changes in the tumour spheres probably resulted in mtDNA depletion, as the cells suppressed mitochondrial respiration and switched to an alternative mode of energy production, i.e. glycolysis. Then, to ascertain the origin of the variation in mtDNA content, we used MinION, a nanopore sequencer, to sequence the mitochondrial genomes of H103, SAS, and the tumour spheres. We found that the lower cisplatin sensitivity of H103 could have been caused by a constellation of genetic and epigenetic changes in its mitochondrial genome. Future work may look into how changes in mtDNA translate into an impact on cell function and therefore cisplatin response.
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