Targeting cancer cells through antibiotics-induced mitochondrial dysfunction requires autophagy inhibition
Language English Country Ireland Media print-electronic
Document type Journal Article
PubMed
27693455
DOI
10.1016/j.canlet.2016.09.023
PII: S0304-3835(16)30565-1
Knihovny.cz E-resources
- Keywords
- Antibiotics, Autophagy, Cancer, Mitochondria, Mitochondrial dysfunction, Mitophagy,
- MeSH
- Adenine analogs & derivatives pharmacology MeSH
- Adenosine Triphosphate metabolism MeSH
- Anti-Bacterial Agents pharmacology MeSH
- Autophagy drug effects MeSH
- Time Factors MeSH
- Electron Transport Chain Complex Proteins metabolism MeSH
- Energy Metabolism drug effects MeSH
- Humans MeSH
- Membrane Potential, Mitochondrial drug effects MeSH
- Mitochondria drug effects metabolism pathology MeSH
- Mitophagy drug effects MeSH
- Cell Line, Tumor MeSH
- Breast Neoplasms drug therapy genetics metabolism pathology MeSH
- Cell Proliferation drug effects MeSH
- Microtubule-Associated Proteins genetics metabolism MeSH
- Antineoplastic Combined Chemotherapy Protocols pharmacology MeSH
- Reactive Oxygen Species metabolism MeSH
- Signal Transduction drug effects MeSH
- Drug Synergism MeSH
- Transfection MeSH
- Check Tag
- Humans MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- 3-methyladenine MeSH Browser
- Adenine MeSH
- Adenosine Triphosphate MeSH
- Anti-Bacterial Agents MeSH
- Electron Transport Chain Complex Proteins MeSH
- Microtubule-Associated Proteins MeSH
- Reactive Oxygen Species MeSH
A significant part of current research studies utilizes various cellular models which imply specific antibiotics-containing media as well as antibiotics used for clonal selection or promoter de/activation. With the great success of developing such tools, mitochondria, once originated from bacteria, can be effectively targeted by antibiotics. For that reason, some studies propose antibiotics-targeting of mitochondria as part of anticancer therapy. Here, we have focused on the effects of various classes of antibiotics on mitochondria in cancer and non-cancer cells and demonlow mitochondrial membrane potential, reduced ATP production, altered morphology and lowered respiration rate which altogether suggested mitochondrial dysfunction (MDF). This was in parallel with increased level of reactive oxygen species (ROS) and decreased activity of mitochondrial respiration complexes. However, both survival and repopulation capacity of cancer cells was not significantly affected by the antibiotics, perhaps due to a glycolytic shift or activated autophagy. In turn, simultaneous inhibition of autophagy and treatment with antibiotics largely reduced tumorigenic properties of cancer cells suggesting potential strategy for anticancer therapy.
Department of Histology and Embryology Faculty of Medicine Masaryk University Brno Czech Republic
Novosibirsk State University Novosibirsk Pirogova 2 630090 Russia
Translational Research in Cancer Stem Cells Vall d'Hebron Institut de Recerca Barcelona Spain
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