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Background: Pancreatic ductal adenocarcinoma (PDA) is currently the 4th leading cause of cancer death in the US because of late detection and resistance to chemotherapy and radiation. This tumor resistance is partially due to high activity of the transcription factor, NF-kB which promotes cell survival and pyruvate dehydrogenase kinase 2 (PDK2) which regulates aerobic glycolysis (Warburg Metabolism), cell proliferation, and inhibition of apoptosis. We have shown that simultaneous treatment with the chemical NF-kB inhibitor DMAPT and the Warburg inhibitor DCA is cytotoxic and enhances radiation-induced cell death in human PDA cells.

Determining if Double Gene Knockdown of P65 and PDK2 Increases Cytotoxicity and Radiation Sensitivity of Pancreatic Cancer Cells