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Difference between revisions of "Chowdhury 2005 Biochem Biophys Res Comm"

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{{Publication
{{Publication
|title=Chowdhury SKR, Gemin A, Singh G (2005) High activity of mitochondrial glycerophosphate dehydrogenase and glycerophosphate-dependent ROS production in prostate cancer cell lines. Biochem. Biophys. Res. Comm. 333: 1139-1145.
|title=Chowdhury SK, Gemin A, Singh G (2005) High activity of mitochondrial glycerophosphate dehydrogenase and glycerophosphate-dependent ROS production in prostate cancer cell lines. Biochem Biophys Res Comm 333:1139-45.
|authors=Chowdhury SKR, Gemin A, Singh G
|info=[http://www.ncbi.nlm.nih.gov/pubmed/15967408 PMID: 15967408]
|authors=Chowdhury SK, Gemin A, Singh G
|year=2005
|year=2005
|journal=Biochem. Biophys. Res. Commun.
|journal=Biochem Biophys Res Commun
|abstract=Most malignant cells are highly glycolytic and produce high levels of reactive oxygen species (ROS) compared to normal cells. Mitochondrial glycerophosphate dehydrogenase (mGPDH) participates in the reoxidation of cytosolic NADH by delivering reducing equivalents from this molecule into the electron transport chain, thus sustaining glycolysis. Here, we investigate the role of mGPDH in maintaining an increased rate of glycolysis and evaluate glycerophosphate-dependent ROS production in prostate cancer cell lines (LNCaP, DU145, PC3, and CL1). Immunoblot, polarographic, and spectrophotometric analyses revealed that mGPDH abundance and activity was significantly elevated in prostate cancer cell lines when compared to the normal prostate epithelial cell line PNT1A. Furthermore, both the glycolytic capacity and glycerophosphate-dependent ROS production was increased 1.68- to 4.44-fold and 5- to 7-fold, respectively, in prostate cancer cell lines when compared to PNT1A cells. Overall, these data demonstrate that mGPDH is involved in maintaining a high rate of glycolysis and is an important site of electron leakage leading to ROS production in prostate cancer cells.
|abstract=Most malignant cells are highly glycolytic and produce high levels of reactive oxygen species (ROS) compared to normal cells. [[Glycerophosphate dehydrogenase complex |Mitochondrial glycerophosphate dehydrogenase]] (mGPDH) participates in the reoxidation of cytosolic NADH by delivering reducing equivalents from this molecule into the electron transport chain, thus sustaining glycolysis. Here, we investigate the role of mGPDH in maintaining an increased rate of glycolysis and evaluate glycerophosphate-dependent ROS production in prostate cancer cell lines (LNCaP, DU145, PC3, and CL1). Immunoblot, polarographic, and spectrophotometric analyses revealed that mGPDH abundance and activity was significantly elevated in prostate cancer cell lines when compared to the normal prostate epithelial cell line PNT1A. Furthermore, both the glycolytic capacity and glycerophosphate-dependent ROS production was increased 1.68- to 4.44-fold and 5- to 7-fold, respectively, in prostate cancer cell lines when compared to PNT1A cells. Overall, these data demonstrate that mGPDH is involved in maintaining a high rate of glycolysis and is an important site of electron leakage leading to ROS production in prostate cancer cells.
|keywords=Mitochondrial glycerophosphate dehydrogenase, Reactive oxygen species, Glycolysis, Glycerophosphate shuttle, Prostate cancer
|keywords=Mitochondrial glycerophosphate dehydrogenase, Reactive oxygen species, Glycolysis, Glycerophosphate shuttle, Prostate cancer
|info=[http://www.ncbi.nlm.nih.gov/pubmed/15967408 PMID: 15967408]
|mipnetlab=CA Hamilton Singh G,
|discipline=Mitochondrial Physiology, Biomedicine
}}
}}
{{Labeling
{{Labeling
|discipline=Mitochondrial Physiology, Biomedicine
|area=Respiration, Genetic knockout;overexpression
|injuries=Cancer; Apoptosis; Cytochrome c, Genetic Defect; Knockdown; Overexpression
|diseases=Cancer
|organism=Human
|organism=Human
|topics=Respiration; OXPHOS; ETS Capacity, Substrate; Glucose; TCA Cycle
|tissues=Genital
|preparations=Permeabilized cells
|topics=Substrate
|couplingstates=LEAK, OXPHOS, ET
|pathways=Gp
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|discipline=Mitochondrial Physiology, Biomedicine
}}
}}

Latest revision as of 19:13, 1 April 2018

Publications in the MiPMap
Chowdhury SK, Gemin A, Singh G (2005) High activity of mitochondrial glycerophosphate dehydrogenase and glycerophosphate-dependent ROS production in prostate cancer cell lines. Biochem Biophys Res Comm 333:1139-45.

Β» PMID: 15967408

Chowdhury SK, Gemin A, Singh G (2005) Biochem Biophys Res Commun

Abstract: Most malignant cells are highly glycolytic and produce high levels of reactive oxygen species (ROS) compared to normal cells. Mitochondrial glycerophosphate dehydrogenase (mGPDH) participates in the reoxidation of cytosolic NADH by delivering reducing equivalents from this molecule into the electron transport chain, thus sustaining glycolysis. Here, we investigate the role of mGPDH in maintaining an increased rate of glycolysis and evaluate glycerophosphate-dependent ROS production in prostate cancer cell lines (LNCaP, DU145, PC3, and CL1). Immunoblot, polarographic, and spectrophotometric analyses revealed that mGPDH abundance and activity was significantly elevated in prostate cancer cell lines when compared to the normal prostate epithelial cell line PNT1A. Furthermore, both the glycolytic capacity and glycerophosphate-dependent ROS production was increased 1.68- to 4.44-fold and 5- to 7-fold, respectively, in prostate cancer cell lines when compared to PNT1A cells. Overall, these data demonstrate that mGPDH is involved in maintaining a high rate of glycolysis and is an important site of electron leakage leading to ROS production in prostate cancer cells. β€’ Keywords: Mitochondrial glycerophosphate dehydrogenase, Reactive oxygen species, Glycolysis, Glycerophosphate shuttle, Prostate cancer

β€’ O2k-Network Lab: CA Hamilton Singh G


Labels: MiParea: Respiration, Genetic knockout;overexpression  Pathology: Cancer 

Organism: Human  Tissue;cell: Genital  Preparation: Permeabilized cells 

Regulation: Substrate  Coupling state: LEAK, OXPHOS, ET  Pathway: Gp  HRR: Oxygraph-2k