Table of Contents Author Guidelines Submit a Manuscript
BioMed Research International
Volume 2015, Article ID 827462, 10 pages
http://dx.doi.org/10.1155/2015/827462
Research Article

Cosuppression of Sprouty and Sprouty-Related Negative Regulators of FGF Signalling in Prostate Cancer: A Working Hypothesis

1Disciplines of Physiology, School of Medical Sciences and Bosch Institute, University of Sydney, Sydney, NSW 2006, Australia
2Anatomy and Histology, School of Medical Sciences and Bosch Institute, University of Sydney, Sydney, NSW 2006, Australia

Received 11 July 2014; Accepted 14 November 2014

Academic Editor: Tarunveer S. Ahluwalia

Copyright © 2015 Stephen J. Assinder et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Linked References

  1. C. G. Roehrborn and L. K. Black, “The economic burden of prostate cancer,” BJU International, vol. 108, no. 6, pp. 806–813, 2011. View at Publisher · View at Google Scholar · View at Scopus
  2. B. Kwabi-Addo, M. Ozen, and M. Ittmann, “The role of fibroblast growth factors and their receptors in prostate cancer,” Endocrine-Related Cancer, vol. 11, no. 4, pp. 709–724, 2004. View at Publisher · View at Google Scholar · View at Scopus
  3. D. Giri, F. Ropiquet, and M. Ittmann, “Alterations in expression of basic fibroblast growth factor (FGF) 2 and its receptor FGFR-1 in human prostate cancer,” Clinical Cancer Research, vol. 5, no. 5, pp. 1063–1071, 1999. View at Google Scholar · View at Scopus
  4. A. Aigner, M. Butscheid, P. Kunkel et al., “An FGF-binding protein (FGF-BP) exerts its biological function by parallel paracrine stimulation of tumor cell and endothelial cell proliferation through FGF-2 release,” International Journal of Cancer, vol. 92, no. 4, pp. 510–517, 2001. View at Google Scholar
  5. K. Sahadevan, S. Darby, H. Y. Leung, M. E. Mathers, C. N. Robson, and V. J. Gnanapragasam, “Selective over-expression of fibroblast growth factor receptors 1 and 4 in clinical prostate cancer,” The Journal of Pathology, vol. 213, no. 1, pp. 82–90, 2007. View at Publisher · View at Google Scholar · View at Scopus
  6. V. D. Acevedo, R. D. Gangula, K. W. Freeman et al., “Inducible FGFR-1 activation leads to irreversible prostate adenocarcinoma and an epithelial-to- mesenchymal transition,” Cancer Cell, vol. 12, no. 6, pp. 559–571, 2007. View at Publisher · View at Google Scholar · View at Scopus
  7. J. Wang, W. Yu, Y. Cai, C. Ren, and M. M. Ittmann, “Altered fibroblast growth factor receptor 4 stability promotes prostate cancer progression,” Neoplasia, vol. 10, no. 8, pp. 847–856, 2008. View at Publisher · View at Google Scholar · View at Scopus
  8. N. Sugiyama, M. Varjosalo, P. Meller et al., “Fibroblast growth factor receptor 4 regulates tumor invasion by coupling fibroblast growth factor signaling to extracellular matrix degradation,” Cancer Research, vol. 70, no. 20, pp. 7851–7861, 2010. View at Publisher · View at Google Scholar · View at Scopus
  9. N. Hacohen, S. Kramer, D. Sutherland, Y. Hiromi, and M. Krasnow, “Sprouty encodes an antagonist of FGF signalling that patterns apical branching of Drosophila airways,” Cell, vol. 9, pp. 219–222, 1998. View at Google Scholar
  10. J. D. Tefft, L. Matt, S. Smith et al., “Conserved function of mSpry-2, a murine homolog of Drosophila sprouty, which negatively modulates respiratory organogenesis,” Current Biology, vol. 9, no. 4, pp. 219–222, 1999. View at Publisher · View at Google Scholar · View at Scopus
  11. D. Chambers and I. Mason, “Expression of sprouty 2 during early development of the chick embryo is coincident with known sites of FGF signalling,” Mechanisms of Development, vol. 91, no. 1-2, pp. 361–364, 2000. View at Publisher · View at Google Scholar · View at Scopus
  12. T. Casci, J. Vinós, and M. Freeman, “Sprouty, an intracellular inhibitor of Ras signaling,” Cell, vol. 96, no. 5, pp. 655–665, 1999. View at Publisher · View at Google Scholar · View at Scopus
  13. G. Minowada, L. A. Jarvis, C. L. Chi et al., “Vertebrate sprouty genes are induced by FGF signaling and can cause chondrodysplasia when overexpressed,” Development, vol. 126, no. 20, pp. 4465–4475, 1999. View at Google Scholar · View at Scopus
  14. M. Fürthauer, F. Reifers, M. Brand, B. Thisse, and C. Thisse, “Sprouty 4 acts in vivo as a feedback-induced antagonist of FGF signalling in Zebrafish,” Development, vol. 128, no. 12, pp. 2175–2186, 2001. View at Google Scholar · View at Scopus
  15. H. Hanafusa, S. Torii, T. Yasunaga, and E. Nishida, “Sprouty1 and Sprouty2 provide a control mechanism for the Ras/MAPK signalling pathway,” Nature Cell Biology, vol. 4, no. 11, pp. 850–858, 2002. View at Publisher · View at Google Scholar · View at Scopus
  16. A. Sasaki, T. Taketomi, R. Kato et al., “Mammalian Sprouty4 suppresses Ras-independent ERK activation by binding to Raf1,” Nature Cell Biology, vol. 5, no. 5, pp. 427–432, 2003. View at Publisher · View at Google Scholar · View at Scopus
  17. P. Yusoff, D. H. Lao, S. H. Ong et al., “Sprouty2 inhibits the Ras/MAP kinase pathway by inhibiting the activation of Raf,” Journal of Biological Chemistry, vol. 277, no. 5, pp. 3195–3201, 2002. View at Publisher · View at Google Scholar · View at Scopus
  18. D. Kovalenko, X. Yang, R. J. Nadeau, L. K. Harkins, and R. Friesel, “Sef inhibits fibroblast growth factor signaling by inhibiting FGFR1 tyrosine phosphorylation and subsequent ERK activation,” The Journal of Biological Chemistry, vol. 278, no. 16, pp. 14087–14091, 2003. View at Publisher · View at Google Scholar · View at Scopus
  19. T. L. Lo, P. Yusoff, C. W. Fong et al., “The ras/mitogen-activated protein kinase pathway inhibitor and likely tumor suppressor proteins, sprouty 1 and sprouty 2 are deregulated in breast cancer,” Cancer Research, vol. 64, no. 17, pp. 6127–6136, 2004. View at Publisher · View at Google Scholar · View at Scopus
  20. C. W. Fong, M.-S. Chua, A. B. McKie et al., “Sprouty 2, an inhibitor of mitogen-activated protein kinase signaling, is down-regulated in hepatocellular carcinoma,” Cancer Research, vol. 66, no. 4, pp. 2048–2058, 2006. View at Publisher · View at Google Scholar · View at Scopus
  21. H. Sutterlüty, C.-E. Mayer, U. Setinek et al., “Down-regulation of Sprouty2 in non-small cell lung cancer contributes to tumor malignancy via extracellular signal-regulated kinase pathway-dependent and -independent mechanisms,” Molecular Cancer Research, vol. 5, no. 5, pp. 509–520, 2007. View at Publisher · View at Google Scholar · View at Scopus
  22. S. A. Lee, C. Ho, R. Roy et al., “Integration of genomic analysis and in vivo transfection to identify sprouty 2 as a candidate tumor suppressor in liver cancer,” Hepatology, vol. 47, no. 4, pp. 1200–1210, 2008. View at Publisher · View at Google Scholar · View at Scopus
  23. G. Minowada and Y. E. Miller, “Overexpression of Sprouty 2 in mouse lung epithelium inhibits urethane-induced tumorigenesis,” American Journal of Respiratory Cell and Molecular Biology, vol. 40, no. 1, pp. 31–37, 2009. View at Publisher · View at Google Scholar · View at Scopus
  24. T. Yoshida, T. Hisamoto, J. Akiba et al., “Spreds, inhibitors of the Ras/ERK signal transduction, are dysregulated in human hepatocellular carcinoma and linked to the malignant phenotype of tumors,” Oncogene, vol. 25, no. 45, pp. 6056–6066, 2006. View at Publisher · View at Google Scholar · View at Scopus
  25. B. Kwabi-Addo, J. Wang, H. Erdem et al., “The expression of Sprouty1, an inhibitor of fibroblast growth factor signal transduction, is decreased in human prostate cancer,” Cancer Research, vol. 64, no. 14, pp. 4728–4735, 2004. View at Publisher · View at Google Scholar · View at Scopus
  26. S. Fritzsche, M. Kenzelmann, M. J. Hoffmann et al., “Concomitant down-regulation of SPRY1 and SPRY2 in prostate carcinoma,” Endocrine-Related Cancer, vol. 13, no. 3, pp. 839–849, 2006. View at Publisher · View at Google Scholar · View at Scopus
  27. J. L. Schutzman and G. R. Martin, “Sprouty genes function in suppression of prostate tumorigenesis,” Proceedings of the National Academy of Sciences of the United States of America, vol. 109, no. 49, pp. 20023–20028, 2012. View at Publisher · View at Google Scholar · View at Scopus
  28. N. Kachroo, T. Valencia, A. Y. Warren, and V. J. Gnanapragasam, “Evidence for downregulation of the negative regulator SPRED2 in clinical prostate cancer,” British Journal of Cancer, vol. 108, no. 3, pp. 597–601, 2013. View at Publisher · View at Google Scholar · View at Scopus
  29. M. A. Basson, S. Akbulut, J. Watson-Johnson et al., “Sprouty1 is a critical regulator of GDNF/RET-mediated kidney induction,” Developmental Cell, vol. 8, no. 2, pp. 229–239, 2005. View at Publisher · View at Google Scholar · View at Scopus
  30. K. Shim, G. Minowada, D. E. Coling, and G. R. Martin, “Sprouty2, a mouse deafness gene, regulates cell fate decisions in the auditory sensory epithelium by antagonizing FGF signaling,” Developmental Cell, vol. 8, no. 4, pp. 553–564, 2005. View at Publisher · View at Google Scholar · View at Scopus
  31. S. B. Shappell, G. V. Thomas, R. L. Roberts et al., “Prostate pathology of genetically engineered mice: definitions and classification. The consensus report from the Bar Harbor meeting of the mouse models of human cancer consortium prostate pathology committee,” Cancer Research, vol. 64, no. 6, pp. 2270–2305, 2004. View at Publisher · View at Google Scholar · View at Scopus
  32. S. Varambally, J. Yu, B. Laxman et al., “Integrative genomic and proteomic analysis of prostate cancer reveals signatures of metastatic progression,” Cancer Cell, vol. 8, no. 5, pp. 393–406, 2005. View at Publisher · View at Google Scholar · View at Scopus
  33. D. K. Vanaja, J. C. Cheville, S. J. Iturria, and C. Y. F. Young, “Transcriptional silencing of zinc finger protein 185 identified by expression profiling is associated with prostate cancer progression,” Cancer Research, vol. 63, no. 14, pp. 3877–3882, 2003. View at Google Scholar · View at Scopus
  34. A. MacIà, M. Vaquero, M. Gou-Fàbregas et al., “Sprouty1 induces a senescence-associated secretory phenotype by regulating NFκB activity: implications for tumorigenesis,” Cell Death & Differentiation, vol. 21, no. 2, pp. 333–343, 2014. View at Publisher · View at Google Scholar · View at Scopus
  35. A. M. De Marzo, A. K. Meeker, S. Zha et al., “Human prostate cancer precursors and pathobiology,” Urology, vol. 62, no. 5, pp. 55–62, 2003. View at Publisher · View at Google Scholar · View at Scopus
  36. M. J. Gerdes, M. Larsen, T. D. Dang, S. J. Ressler, J. A. Tuxhorn, and D. R. Rowley, “Regulation of rat prostate stromal cell myodifferentiation by androgen and TGF-β1,” Prostate, vol. 58, no. 3, pp. 299–307, 2004. View at Publisher · View at Google Scholar · View at Scopus
  37. F. Yang, J. A. Tuxhorn, S. J. Ressler, S. J. McAlhany, T. D. Dang, and D. R. Rowley, “Stromal expression of connective tissue growth factor promotes angiogenesis and prostate cancer tumorigenesis,” Cancer Research, vol. 65, no. 19, pp. 8887–8895, 2005. View at Publisher · View at Google Scholar · View at Scopus
  38. E. H. H. Shin, M. A. Basson, M. L. Robinson, J. W. McAvoy, and F. J. Lovicu, “Sprouty is a negative regulator of transforming growth factor β-induced epithelial-to-mesenchymal transition and cataract,” Molecular Medicine, vol. 18, pp. 861–873, 2012. View at Google Scholar · View at Scopus
  39. F. Yang, D. W. Strand, and D. R. Rowley, “Fibroblast growth factor-2 mediates transforming growth factor-β action in prostate cancer reactive stroma,” Oncogene, vol. 27, no. 4, pp. 450–459, 2008. View at Publisher · View at Google Scholar · View at Scopus
  40. S. Wang, A. J. Garcia, M. Wu, D. A. Lawson, O. N. Witte, and H. Wu, “Pten deletion leads to the expansion of a prostatic stem/progenitor cell subpopulation and tumor initiation,” Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 5, pp. 1480–1485, 2006. View at Publisher · View at Google Scholar · View at Scopus
  41. F. Edwin, R. Singh, R. Endersby, S. J. Baker, and T. B. Patel, “The tumor suppressor PTEN is necessary for human sprouty 2-mediated inhibition of cell proliferation,” The Journal of Biological Chemistry, vol. 281, no. 8, pp. 4816–4822, 2006. View at Publisher · View at Google Scholar · View at Scopus