G-protein-coupled receptor agonist BV8/prokineticin-2 and STAT3 protein form a feed-forward loop in both normal and malignant myeloid cells

Abstract

Background: Signaling pathways underlying BV8-mediated oncogenesis remain unknown. Results: BV8-STAT3 forms a feed-forward loop in both normal and malignant myeloid cells and promotes tumor growth. Conclusion: JAK2/STAT3 signaling plays critical roles in BV8-mediated myeloid cell-dependent oncogenesis. Significance: This study identifies a novel role of BV8-STAT3 signaling in mediating cross-talk between tumor microenvironment and tumor cells. Copyright © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.