ArticleThe Journal of biological chemistry2011
Mitochondrial dysfunction in cancer cells due to aberrant mitochondrial replication.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 77 citations in OpenAlex.
- A Fluid Dynamics-Model System for Advancing Tissue Engineering and Cancer Research Studies: Biological Assessment of the Innovative BioAxFlow Dynamic Culture Bioreactor.Biomimetics (Basel, Switzerland) · 2025Article
- Polyphenols and Exercise in Mitochondrial Biogenesis: Focus on Age-Related CNS Disorders.Molecular neurobiology · 2025Review
- Uncovering differential gene expression between mtRNA-positive and -negative osteosarcoma cells: implications beyond mitochondrial function.Frontiers in genetics · 2025Article
- Deregulation of mitochondrial gene expression in cancer: mechanisms and therapeutic opportunities.British journal of cancer · 2024Review
- Aberrant LETM1 elevation dysregulates mitochondrial functions and energy metabolism and promotes lung metastasis in osteosarcoma.Genes & diseases · 2024Article
- Comprehensive pan-cancer analysis reveals CCDC58 as a carcinogenic factor related to immune infiltration.Apoptosis : an international journal on programmed cell death · 2024Article
- Metabolic reprogramming in osteosarcoma.Pediatric discovery · 2023Review
- Identification of SSBP1 as a ferroptosis-related biomarker of glioblastoma based on a novel mitochondria-related gene risk model and in vitro experiments.Journal of translational medicine · 2022Article
- Electromagnetic stimulation increases mitochondrial function in osteogenic cells and promotes bone fracture repair.Scientific reports · 2021Article
- Targeting cancer-cell mitochondria and metabolism to improve radiotherapy response.Translational oncology · 2021Review
- Pathogenic mutations reveal a role of RECQ4 in mitochondrial RNA:DNA hybrid formation and resolution.Scientific reports · 2020Article
- The RNA helicase DDX5 supports mitochondrial function in small cell lung cancer.The Journal of biological chemistry · 2020Article
- Intramitochondrial Src kinase links mitochondrial dysfunctions and aggressiveness of breast cancer cells.Cell death & disease · 2019Article
- Photostable, hydrophilic, and near infrared quaterrylene-based dyes for photoacoustic imaging.Materials science & engineering. C, Materials for biological applications · 2018Article
- Vnn1 pantetheinase limits the Warburg effect and sarcoma growth by rescuing mitochondrial activity.Life science alliance · 2018Article
- A functional polymorphism ofOncotarget · 2017Article
- Epigenetic modification of miR-663 controls mitochondria-to-nucleus retrograde signaling and tumor progression.The Journal of biological chemistry · 2017Article
- Prediction ofSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2017Article
- miR‑4262 inhibits colon cancer cell proliferation via targeting of GALNT4.Molecular medicine reports · 2017Article
- Mitochondrial deficiency impairs hypoxic induction of HIF-1 transcriptional activity and retards tumor growth.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Warburg effect is a hallmark of cancer manifested by continuous prevalence of glycolysis and dysregulation of oxidative metabolism. Glycolysis provides survival advantage to cancer cells. To investigate molecular mechanisms underlying the Warburg effect, we first compared oxygen consumption among hFOB osteoblasts, benign osteosarcoma cells, Saos2, and aggressive osteosarcoma cells, 143B. We demonstrate that, as both proliferation and invasiveness increase in osteosarcoma, cells utilize significantly less oxygen. We proceeded to evaluate mitochondrial morphology and function. Electron microscopy showed that in 143B cells, mitochondria are enlarged and increase in number. Quantitative PCR revealed an increase in mtDNA in 143B cells when compared with hFOB and Saos2 cells. Gene expression studies showed that mitochondrial single-strand DNA-binding protein (mtSSB), a key catalyst of mitochondrial replication, was significantly up-regulated in 143B cells. In addition, increased levels of the mitochondrial respiratory complexes were accompanied by significant reduction of their activities. These changes indicate hyperactive mitochondrial replication in 143B cells. Forced overexpression of mtSSB in Saos2 cells caused an increase in mtDNA and a decrease in oxygen consumption. In contrast, knockdown of mtSSB in 143B cells was accompanied by a decrease in mtDNA, increase in oxygen consumption, and retardation of cell growth in vitro and in vivo. In summary, we have found that mitochondrial dysfunction in cancer cells correlates with abnormally increased mitochondrial replication, which according to our gain- and loss-of-function experiments, may be due to overexpression of mtSSB. Our study provides insight into mechanisms of mitochondrial dysfunction in cancer and may offer potential therapeutic targets.
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