wnt5a-nfat signaling mediates resistance to apoptosis in pancreatic cancer

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ID: 180290
2013
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Abstract
INTRODUCTION: WNT5A belongs to the Wnt family of secreted signaling molecules. Using transcriptional profiling, we previously identified WNT5A as target of the antiapoptotic transcription factor CUX1 and demonstrated high expression levels in pancreatic cancer. However, the impact of WNT5A on drug resistance and the signaling pathways employed by WNT5A remain to be elucidated. OBJECTIVES: This project aims to decipher the impact of WNT5A on resistance to apoptosis and the signaling pathways employed by WNT5A in pancreatic cancer. METHODS: The impact of WNT5A and its downstream effectors on tumor growth and drug resistance was studied in vitro and in xenograft models in vivo. Tissue microarrays of pancreatic cancer specimens were employed for immuno-histochemical studies. RESULTS: Knockdown of WNT5A results in a significant increase in drug-induced apoptosis. In contrast, overexpression of WNT5A or addition of recombinant WNT5A mediates resistance to apoptosis in vitro. In our attempt to identify downstream effectors of WNT5A, we identified the transcription factor nuclear factor of activated T cells c2 (NFATc2) as transcriptional target of WNT5A signaling. NFATc2 confers a strong antiapoptotic phenotype mediating at least in part the effects of WNT5A on drug resistance and tumor cell survival. In vivo, WNT5A expression leads to resistance to gemcitabine-induced apoptosis in a xenograft model, which is paralleled by up-regulation of NFATc2. Both WNT5A and NFATc2 proteins are highly expressed in human pancreatic cancer tissues and their expression levels correlated significantly. CONCLUSION: We identified the WNT5A-NFATc2 axis as important mediator of drug resistance in pancreatic cancer.
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griesmann2013neoplasia:wnt5a-nfat Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Heidi Griesmann;Stefanie Ripka;Moritz Pralle;Volker Ellenrieder;Sandra Baumgart;Malte Buchholz;Christian Pilarsky;Daniela Aust;Thomas M. Gress;Patrick Michl
Journal ACS chemical neuroscience
Year 2013
DOI
10.1593/neo.121312
URL
http://www.sciencedirect.com/science/article/pii/S1476558613801224
Keywords
neoplasms Oncology including cancer and carcinogens tumors

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