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  1. Oncogenesis
  2. Year: 2016, Volume: 5
  3. Year: 2016, Volume: 5, Issue: 1
  4. Energy disruptors: rising stars in anticancer therapy?
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Year: 2016, Volume: 5
Year: 2016, Volume: 5, Issue: 4
Year: 2016, Volume: 5, Issue: 1
Mieap-regulated mitochondrial quality control is frequently inactivated in human colorectal cancer
The CaSm (LSm1) oncogene promotes transformation, chemoresistance and metastasis of pancreatic cancer cells
A mix of S and ΔS variants of STAT3 enable survival of activated B-cell-like diffuse large B-cell lymphoma cells in culture
Mucin 1-mediated chemo-resistance in lung cancer cells
Uncoupling of EGFR–RAS signaling and nuclear localization of YBX1 in colorectal cancer
Energy disruptors: rising stars in anticancer therapy?
Lipid metabolic reprogramming in cancer cells
Hypoxia and metabolic adaptation of cancer cells
Year: 2015, Volume: 4
Year: 2015, Volume: 3
Year: 2014, Volume: 3
Year: 2013, Volume: 2
Year: 2012, Volume: 1

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Energy disruptors: rising stars in anticancer therapy?

Content Provider PubMed Central
Author Bost, F. Decoux-poullot, A-g Tanti, J. F. Clavel, S.
Copyright Year 2016
Abstract The metabolic features of tumor cells diverge from those of normal cells. Otto Warburg was the first to observe that cancer cells dramatically increase their glucose consumption to generate ATP. He also claimed that cancer cells do not have functional mitochondria or oxidative phosphorylation (OXPHOS) but simply rely on glycolysis to provide ATP to the cell, even in the presence of oxygen (aerobic glycolysis). Several studies have revisited this observation and demonstrated that most cancer cells contain metabolically efficient mitochondria. Indeed, to sustain high proliferation rates, cancer cells require functional mitochondria to provide ATP and intermediate metabolites, such as citrate and cofactors, for anabolic reactions. This difference in metabolism between normal and tumors cells causes the latter to be more sensitive to agents that can disrupt energy homeostasis. In this review, we focus on energy disruptors, such as biguanides, 2-deoxyglucose and 5-aminoimidazole-4-carboxamide ribonucleotide, that interfere with the main metabolic pathways of the cells, OXPHOS, glycolysis and glutamine metabolism. We discuss the preclinical data and the mechanisms of action of these disruptors at the cellular and molecular levels. Finally, we consider whether these drugs can reasonably contribute to the antitumoral therapeutic arsenal in the future.
Related Links http://dx.doi.org/10.1038/oncsis.2015.46
Starting Page 188
File Format PDF
ISSN 21579024
e-ISSN 21579024
Journal Oncogenesis
Issue Number 1
Volume Number 5
Language English
Publisher Nature Publishing Group
Publisher Date 2016-01-01
Access Restriction Open
Rights Holder Nature Publishing Group
Subject Keyword Research in Higher Education
Content Type Text
Resource Type Article
Subject Molecular Biology Cancer Research
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