ArticleCancer science2009
Mutations in the mitochondrial genome confer resistance of cancer cells to anticancer drugs.
Article in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.
- The Role of Mitochondrial DNA Variation in Drug Response: A Systematic Review.Frontiers in genetics · 2021Pooled it
- Molecular oncology focus - is carcinogenesis a 'mitochondriopathy'?Journal of biomedical science · 2010Pooled it
- Revealing the landscape of targeting mitochondrial functions and behaviors to overcome cancer chemoresistance.Journal of the National Cancer Center · 2025Review
- Mitochondrial transfer in PC-3 cells fingerprinted in ferroptosis sensitivity: a brand new approach targeting cancer metabolism.Human cell · 2023Article
- Genetic mutations affecting mitochondrial function in cancer drug resistance.Genes & genomics · 2023Review
- The mitochondrial unfolded protein response (UPRJournal of hematology & oncology · 2022Review
- Mitochondrial DNA mutations are involved in the acquisition of cisplatin resistance in human lung cancer A549 cells.Oncology reports · 2022Article
- Mitochondrial genome and its regulator TFAM modulates head and neck tumourigenesis through intracellular metabolic reprogramming and activation of oncogenic effectors.Cell death & disease · 2021Article
- Tunneling nanotubes, TNT, communicate glioblastoma with surrounding non-tumor astrocytes to adapt them to hypoxic and metabolic tumor conditions.Scientific reports · 2021Article
- Review
- Quantitative analysis of mitochondrial membrane potential heterogeneity in unsynchronized and synchronized cancer cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Review
- Differential effects of cisplatin on cybrid cells with varying mitochondrial DNA haplogroups.PeerJ · 2020Article
- Mitochondrial Genome (mtDNA) Mutations that Generate Reactive Oxygen Species.Antioxidants (Basel, Switzerland) · 2019Review
- TheGenes · 2018Review
- Mitochondrial Heterogeneity.Frontiers in genetics · 2018Review
- Mitochondrial genome variability: the effect on cellular functional activity.Therapeutics and clinical risk management · 2018Review
- Cisplatin selects short forms of the mitochondrial DNA OriB variant (16184-16193 poly-cytosine tract), which confer resistance to cisplatin.Scientific reports · 2017Article
- Erythrocytosis in hepatocellular carcinoma portends poor prognosis by respiratory dysfunction secondary to mitochondrial DNA mutations.Hepatology (Baltimore, Md.) · 2017Article
- Analysis to Estimate Genetic Variations in the Idarubicin-Resistant Derivative MOLT-3.International journal of molecular sciences · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The majority of cancer cells harbor homoplasmic somatic mutations in the mitochondrial genome. We show here that mutations in mitochondrial DNA (mtDNA) are responsible for anticancer drug tolerance. We constructed several trans-mitochondrial hybrids (cybrids) with mtDNA derived from human pancreas cancer cell lines CFPAC-1 and CAPAN-2 as well as from healthy individuals. These cybrids contained the different mitochondrial genomes with the common nuclear background. We compared the mutant and wild-type cybrids for resistance against an apoptosis-inducing reagent and anticancer drugs by exposing the cybrids to staurosporine, 5-fluorouracil, and cisplatin in vitro, and found that all mutant cybrids were more resistant to the apoptosis-inducing and anticancer drugs than wild-type cybrids. Next, we transplanted mutant and wild-type cybrids into nude mice to generate tumors. Tumors derived from mutant cybrids were more resistant than those from wild-type cybrids in suppressing tumor growth and inducing massive apoptosis when 5-fluorouracil and cisplatin were administered. To confirm the tolerance of mutant cybrids to anticancer drugs, we transplanted a mixture of mutant and wild-type cybrids at a 1:1 ratio into nude mice and examined the effect by the drugs on the drift of the ratio of mutant and wild-type mtDNA. The mutant mtDNA showed better survival, indicating that mutant cybrids were more resistant to the anticancer drugs. Thus, we propose that mutations in the mitochondrial genome are potential targets for prognosis in the administration of anticancer drugs to cancer patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.