Difference between revisions of "Scatena 2017 Abstract MITOEAGLE Barcelona"
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|authors= | |authors=Scatena R, Bottoni P | ||
|year=2017 | |year=2017 | ||
|event=MITOEAGLE Barcelona 2017 | |event=MITOEAGLE Barcelona 2017 | ||
|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]] | |abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]] | ||
Recent data confirm that PPAR-ligands, like metformin, may cause erosion of cancer stem cells (CSCs), also called tumor initiating cells (TICs) or stem like cancer cells ''in vivo'' and ''in vitro'' [1]). Intriguingly, this effect seems to depend on a derangement of mitochondrial respiratory chain, specifically at level of complex I. CSC play a pivotal role in cancer initiation, metastasis and recurrence, as well as in resistance to therapy. On the other side, deep metabolic characterization of these tumorigenic cells revealed a strict dependency on mitochondrial respiration versus glycolysis, suggesting the existence of a common metabolic program active in these slow cycling cancer cells across different tumors. In facts, when OXPHOS activity is suppressed, these cancer cells change their behavior and phenotype showing a dramatic reduction in tumorigenic potential. Hence, the study of the molecular interrelationships among iatrogenic complex I derangement and CSC targeting must become a focus of contemporary research, not only from a therapeutic point of view, but also for a fundamental advance of the molecular biology of cancer in general. | |||
However, a correct methodological approach does require a careful evaluation of mitochondrial respiratory pathophysiology by adopting protocols, technologies and standard procedures really accurate, appropriate, sensitive and above all specific. The advantages and disadvantages with isolated mitochondria and intact cells approaches in hepatocarcinoma could be an illustrative example. | |||
|editor=[[Kandolf G]], | |||
}} | |||
{{Labeling | |||
|area=Respiration | |||
|diseases=Cancer | |||
|tissues=Liver | |||
|preparations=Intact cells, Isolated mitochondria | |||
|enzymes=Complex I | |||
|event=A1 | |||
}} | }} | ||
== Affiliations == | == Affiliations == | ||
:::: Inst Biochem Clinical Biochem, Catholic Univ, Rome Italy | :::: Inst Biochem Clinical Biochem, Catholic Univ, Rome Italy | ||
Revision as of 12:24, 27 February 2017
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Link: MITOEAGLE
Event: MITOEAGLE Barcelona 2017
Recent data confirm that PPAR-ligands, like metformin, may cause erosion of cancer stem cells (CSCs), also called tumor initiating cells (TICs) or stem like cancer cells in vivo and in vitro [1]). Intriguingly, this effect seems to depend on a derangement of mitochondrial respiratory chain, specifically at level of complex I. CSC play a pivotal role in cancer initiation, metastasis and recurrence, as well as in resistance to therapy. On the other side, deep metabolic characterization of these tumorigenic cells revealed a strict dependency on mitochondrial respiration versus glycolysis, suggesting the existence of a common metabolic program active in these slow cycling cancer cells across different tumors. In facts, when OXPHOS activity is suppressed, these cancer cells change their behavior and phenotype showing a dramatic reduction in tumorigenic potential. Hence, the study of the molecular interrelationships among iatrogenic complex I derangement and CSC targeting must become a focus of contemporary research, not only from a therapeutic point of view, but also for a fundamental advance of the molecular biology of cancer in general.
However, a correct methodological approach does require a careful evaluation of mitochondrial respiratory pathophysiology by adopting protocols, technologies and standard procedures really accurate, appropriate, sensitive and above all specific. The advantages and disadvantages with isolated mitochondria and intact cells approaches in hepatocarcinoma could be an illustrative example.
• Bioblast editor: Kandolf G
Labels: MiParea: Respiration Pathology: Cancer
Tissue;cell: Liver
Preparation: Intact cells, Isolated mitochondria
Enzyme: Complex I
Event: A1
Affiliations
- Inst Biochem Clinical Biochem, Catholic Univ, Rome Italy
