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• W2003747297 abstract "Pancreatic ductal adenocarcinoma (PDAC) is the most common cancer of the pancreas, comprising over 85% of all cases. PDAC has a relative 1-year survival rate of 20% and a 5-year survival rate of 4%, making it the fourth most common cause of cancer deaths in the United States. The presence of oncogenically mutated K-RAS in 90% of human PDAC strongly suggests a critical role for this genetic mutation in the development of this disease. However, there are no anti-Ras therapies that have successfully reached the clinic. A better understanding of the molecular mechanisms leading to the development of pancreatic cancer remains a major goal for defining appropriate treatment strategies and early detection. Studies have shown that members of the oncogenic Pim kinase family (Pim-1, Pim-2, and Pim-3) are aberrantly expressed in a variety of solid tumors, including pancreatic cancer. They phosphorylate a host of substrates involved in numerous cellular events, including apoptosis and cell cycle progression. One of the recent substrates found to be phosphorylated by Pim kinases include RUNX transcription factors. Past studies have shown that the Runt-related (RUNX) family of transcription factors (RUNX1, RUNX2, and RUNX3) are involved in cell proliferation and development and expressed in many types of cancers. To attempt to address these observations, we investigated the role of Pim kinases and RUNX proteins, specifically RUNX3, in growth transformation of pancreatic cancer. We hypothesize that decreased expression or phosphorylation of RUNX3 by Pim kinases will be effective in antagonizing the aberrant growth of PDAC. Initially, we demonstrated by western blotting that RUNX3 is expressed in PDAC cell lines and tissues. Also, we found that overexpression or inhibition of oncogenic KRAS correlated with Pim kinases and RUNX3 expression in cell lines, suggesting an important role for K-Ras signaling. Inhibition of RUNX3 by shRNA resulted in a reduction in anchorage-dependent and -independent growth. Additionally, we used a Pim kinase inhibitor to decrease phosphorylation of RUNX3, leading to decrease cell viability of PDAC cells. Results from our studies help characterize the role K-Ras activation plays on the Pim kinase-RUNX3 signaling pathway as it relates to PDAC growth. Furthermore, these findings will allow us to critically validate Pim kinases and RUNX3 as potential targets for drug therapy in pancreatic cancer. Citation Format: Michael G. Cobb, Dana M. Austin, Dapeng Xu, Antonio T. Baines. The role of Pim kinases and RUNX transcription factors as potential molecular targets of K-Ras signaling in pancreatic cancer cells. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Progress and Challenges; Jun 18-21, 2012; Lake Tahoe, NV. Philadelphia (PA): AACR; Cancer Res 2012;72(12 Suppl):Abstract nr B56." @default.
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• W2003747297 date "2012-07-15" @default.
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• W2003747297 title "Abstract B56: The role of Pim kinases and RUNX transcription factors as potential molecular targets of K-Ras signaling in pancreatic cancer cells." @default.
• W2003747297 doi "https://doi.org/10.1158/1538-7445.panca2012-b56" @default.
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