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Abstract 924: GM-CSF induces CREB signaling pathways and modulates tobacco carcinogen-induced pancreatic tumorigenesis
Introduction: Nicotine and nitrosamine exposure from smoking causes pancreatic cell injury and contributes to a cascade of oncogenic events that may be contributing to the rising rate of pancreatic cancer (PDAC). Cytokines activate kinases and transcription factors including cyclic AMP response element binding (CREB) protein. CREB activation through phosphorylation regulates diverse cellular responses. We studied whether granulocyte-macrophage colony stimulating factor (GM-CSF)-dependent phosphorylated CREB plays a role in smoking-induced pathogenesis of PDAC.Experimental procedure: Human tissue microarray analysis was per...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Castellanos, J., Honnenahally, K., Shi, C., Merchant, N., Nagathihalli, N. Tags: Carcinogenesis Source Type: research

Abstract 4456: Aurora-A is a downstream target of RAS and forms a positive feedback regulation loop with NF-{kappa}B in non-small cell lung cancer
Previous studies have shown that inhibition of Aurora-A reduces mutant RAS oncogenic activity and that both Aurora-A and RAS activate NF-κB pathway through phosphorylation of IkBa and upregulation of GSKa, respectively. Here we show that Aurora-A expression and kinase activity are regulated by activating mutation of KRAS. Blockage of NF-κB by IκB-S32/36A abrogated KRAS-induced Aurora-A expression and kinase activity. Furthermore, we demonstrated that NF-κB directly bound to Aurora-A promoter and induces Aurora-A transcription. In addition, depletion of Aurora-A by siRNA and pharmacological inhibitor MLN8237 suppresses ...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Kim, D., Kanai, M., Zheng, X., Zheng, D., Coppola, D., Cheng, J. Q. Tags: Molecular and Cellular Biology Source Type: research

VAChT Inhibition and Bronchioalveolar Carcinoma
In this study, we show that human BACs produce acetylcholine (ACh) and contain several cholinergic factors including acetylcholinesterase (AChE), choline acetyltransferase (ChAT), choline transporter 1 (CHT1, SLC5A7), vesicular acetylcholine transporter (VAChT, SLC18A3), and nACh receptors (AChRs, CHRNAs). Nicotine increased the production of ACh in human BACs, and ACh acts as a growth factor for these cells. Nicotine-induced ACh production was mediated by α7-, α3β2-, and β3-nAChRs, ChAT and VAChT pathways. We observed that nicotine upregulated ChAT and VAChT. Therefore, we conjectured that VAChT antagonists, such as v...
Source: Cancer Research - February 14, 2013 Category: Cancer & Oncology Authors: Lau, J. K., Brown, K. C., Thornhill, B. A., Crabtree, C. M., Dom, A. M., Witte, T. R., Hardman, W. E., McNees, C. A., Stover, C. A., Carpenter, A. B., Luo, H., Chen, Y. C., Shiflett, B. S., Dasgupta, P. Tags: Molecular and Cellular Pathobiology Source Type: research