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Radiation-induced Pancreatic Cancer Cell Killing by Simultaneous Inhibition of NF-kB and Warburg Metabolism by Marc Mendonca is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

What is Radiation-induced Pancreatic Cancer Cell Killing by Simultaneous Inhibition of NF-kB and Warburg Metabolism about?

Low survival rates of pancreatic ductal adenocarcinoma (PDAC) are attributed to its detection at advanced stage and to high chemotherapy and radiation resistance. Previous work has shown that resistance to radiation therapy in other cancers can be decreased through either inhibition of the anti-apoptotic NF-κB cell survival signaling pathway by dimethylaminoparthenolide (DMAPT) or by inhibition of Warburg cancer metabolism with dichloroacetate (DCA). NF-κB promotes cell survival, tumor progression, angiogenesis, and reduces susceptibility to apoptosis. Warburg cancer metabolism is an alternative metabolic pathway that uses lactate rather than oxidative phosphorylation and increases synthesis of cellular molecular precursors that support increased cancer cell growth. We show here that only simultaneous inhibition of NF-κB and Warburg cancer metabolism (aerobic glycolysis) by treatment with (DMAPT) and Dichloroacetate (DCA) and/or siRNA in PDAC cells: slows cell growth, induces cytotoxicity, inhibits autophagy and increases single and fractionated radiation-induced cell killing. In addition, we show by gH2AX foci analyses that simultaneous inhibition of NF-κB (p65 RelA) and pyruvate

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Author

Marc Mendonca

Publisher

Elsevier BV

Published

2022

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)