Abstract
Abstract Epithelial to mesenchymal transition (EMT) is a fundamental cellular process preceding movement. Malignant transformation of epithelial cells also undergo EMT leading to metastasis and a worse prognosis for human cancer patients. Understanding molecular pathways that are linked to EMT may provide additional drug targets to treat epithelial cancers like prostate cancer. Vasoactive intestinal peptide signaling through one of its naturally occurring G-protein coupled receptors, termed VPAC1, induces non-tumor and tumorigenic epithelial cell lines (RWPE-1, LnCaP and PC3 cells) to undergo EMT and downregulate E-cadherin, a hallmark for EMT. Curcumin, an anti-inflammatory molecule, blocked these VIP EMT effects suggesting a role for NF-kB signaling. Our group has uncovered EMT-associated molecular mRNA targets induced by VIP treatment of primary, resting CD4 T cells, including the EMT master regulator transcription factor, SNAIL1. We hypothesize that EMT transition effects by VIP signaling may also involve the upregulation of SNAIL1 protein. To this end, we plan on treating PC3 cells with varying levels of VIP over time (0–24 hr) and measure by immunoblots the extent to which Snail1 protein, and up to 10 additional EMT-associated proteins, are differentially altered. Successful completion of this research is expected to uncover important VIP protein targets that is expected to better explain its epithelial tumorigenic potential.
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