Panov 2011 Abstract IOC65

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Panov A, Orynbayeva Z (2011) The bioenergetic signature of prostate cancer. MiPNet16.03.

Link: MiPNet16.03 IOC65 Abstracts

Panov A, Orynbayeva Zulfiya (2011)

Event: IOC65

The contribution of energy metabolism in cancer development and progression has been reported in number of works [1]. While there are plenty of data which indicates that progression of both primary and metastatic prostatic tumors are determined by the loss of the cell’s apoptotic potential [2], overall not much is known about mitochondrial functions of normal or cancerous prostatic cells, except for the differences in their metabolism of citric acid. Recently it has been shown that alterations in metabolic activities of human prostate LNCaP, DU145 and PC3 cells related to mitochondria dysfunctions [3], while the detail mechanisms of the mitochondria pathology of prostate cancer remain uncertain. It is important to understand biochemical and physiological aspects of mitochondria functionality as a central gate-keeper in inability of prostate cancer cells to commit to programmed cell death. We report here that mitochondria, from the three metastatic PC cell lines studied, have a number of distinct metabolic features: higher electrical membrane potential, low affinity of the Complex I to NADH, higher resistance to Ca2+ loads, and an unusual response to cyclosporine A when compared with PrEC prostate benign cell mitochondria. The observed metabolic features of mitochondria may protect the prostate cancer cells from apoptosis by direct and indirect inhibition of mitochondria PT.

Keywords: Prostate cancer, Mitochondria metabolism, Apoptosis

O2k-Network Lab: US PA Philadelphia Orynbayeva Z


Labels: Pathology: Cancer 







Authors: Panov A (1), Orynbayeva Zulfiya (2)

Affiliations: (1) WellStar College of Health & Human Services, Kennesaw State University, USA. (2) Department of Surgery, Drexel University College of Medicine, USA.

References: 1. Moreno-Sanchez, R., S. Rodriguez-Enriquez, et al. (2007). Energy metabolism in tumor cells. FEBS J 274(6): 1393-1418. 2. Hail, N., Jr., P. Chen, et al. (2009). Selective apoptosis induction by the cancer chemopreventive agent N-(4-hydroxyphenyl)retinamide is achieved by modulating mitochondrial bioenergetics in premalignant and malignant human prostate epithelial cells. Apoptosis 14(7): 849-863. 3. Higgins, L. H., H. G. Withers, et al. (2009). Hypoxia and the metabolic phenotype of prostate cancer cells. Biochim Biophys Acta 1787(12): 1433-1443.