Background: A low quantity of mitochondrial DNA (mtDNA) is a risk factor in a variety of tumor types. However, it is unclear how mtDNA reduction influences tumor behavior.
Material and methods: mtDNA-deficient ovarian cancer cells were established by ethidium bromide (EtBr) treatment with additive combination of pyruvate and uridine.
Results: The mtDNA-deficient cells had a low growth and colony-forming efficiency compared to the control cells. RNA sequencing revealed down-regulation of mitochondrion-related genes and up-regulation of genes related to cell proliferation and anti-apoptosis. The expression of genes involved in cancer metastasis, proliferation, angiogenesis, drug resistance and cancer cell stemness were also up-regulated. Intriguingly, cancer stem cell markers CD90 and CD117 were both up-regulated by EtBr dose-dependently in both cell lines.
Conclusion: MtDNA deficiency may induce ovarian cancer stem cell-like properties through different ways in vitro, therefore contributing to different tumor behaviors.
Keywords: CSCs; Mitochondrion; RT-PCR; anti-apoptosis; cancer cell proliferation; cancer stem cells; immunocytochemistry; mitochondrial DNA deficiency/dysfunction; stemness; transcriptome sequencing/RNA deep-sequencing; western blotting.
Copyright© 2015 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.