Inositol Polyphosphate-5-Phosphatase F (INPP5F) inhibits STAT3 activity and suppresses gliomas tumorigenicity

Scientific Reports

Volumn 4, Issue , 2014, Pages

  Kim, Hong Sug ^a   Li, Aiguo ^a   Ahn, Susie ^a   Song, Hua ^a   Zhang, Wei ^a  

^a NATIONAL CANCER INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

INOSITOL-POLYPHOSPHATE 5-PHOSPHATASE; PHOSPHATASE; STAT3 PROTEIN; STAT3 PROTEIN, HUMAN;

BRAIN TUMOR; CARCINOGENESIS; CELL PROLIFERATION; CELL SURVIVAL; EPIDEMIOLOGY; GLIOBLASTOMA; HUMAN; METABOLISM; MORTALITY; PHOSPHORYLATION; RISK ASSESSMENT; SIGNAL TRANSDUCTION; SURVIVAL RATE; UNITED STATES;

BRAIN NEOPLASMS; CARCINOGENESIS; CELL PROLIFERATION; CELL SURVIVAL; GLIOBLASTOMA; HUMANS; PHOSPHORIC MONOESTER HYDROLASES; PHOSPHORYLATION; RISK ASSESSMENT; SIGNAL TRANSDUCTION; STAT3 TRANSCRIPTION FACTOR; SURVIVAL RATE; UNITED STATES;

EID: 84923376487     PISSN: None     EISSN: 20452322     Source Type: Journal    
DOI: 10.1038/srep07330     Document Type: Article

References (34)

1. Gilbert, M. R. et al. A randomized trial of bevacizumab for newly diagnosed glioblastoma. N Engl J Med 370, 699-708 (2014).
2. Ohgaki, H. & Kleihues, P. Genetic pathways to primary and secondary glioblastoma. Am J Pathol 170, 1445-1453 (2007).
3. Minagawa, T., Ijuin, T., Mochizuki, Y. & Takenawa, T. Identification and characterization of a sac domain-containing phosphoinositide 5-phosphatase. J Biol Chem 276, 22011-22015 (2001).
4. Trivedi, C. M. et al. Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3 beta activity. Nat Med 13, 324-331 (2007).
5. Zhu, W. et al. Inpp5f is a polyphosphoinositide phosphatase that regulates cardiac hypertrophic responsiveness. Circ Res 105, 1240-1247 (2009).
6. Frank, D. A. STAT signaling in the pathogenesis and treatment of cancer. Mol Med 5, 432-456 (1999).
7. Frank, D. A. STAT3 as a central mediator of neoplastic cellular transformation. Cancer Lett 251, 199-210 (2007).
8. Bromberg, J. F., Horvath, C.M., Besser,D., Lathem,W.W. Darnell, J. E., Jr. Stat3 activation is required for cellular transformation by v-src. Mol Cell Biol 18, 2553-2558 (1998).
9. Turkson, J. et al. Stat3 activation by Src induces specific gene regulation and is required for cell transformation. Mol Cell Biol 18, 2545-2552 (1998).
10. Bromberg, J. F. et al. Stat3 as an oncogene. Cell 98, 295-303 (1999).
11. Reich, N. C. Liu, L. Tracking STAT nuclear traffic. Nat Rev Immunol 6, 602-612 (2006).
12. Ma, J., Zhang, T., Novotny-Diermayr, V., Tan, A. L.& Cao, X. A novel sequence in the coiled-coil domain of Stat3 essential for its nuclear translocation. J Biol Chem 278, 29252-29260 (2003).
13. Ma, J. & Cao, X. Regulation of Stat3 nuclear import by importin alpha5 and importin alpha7 via two different functional sequence elements. Cell Signal 18, 1117-1126 (2006).
14. Network, T. C. G. A. R. Comprehensive genomic characterization defines human glioblastoma genes and core pathways. Nature 455, 1061-1068 (2008).
15. Madhavan, S. et al. Rembrandt: helping personalized medicine become a reality through integrative translational research. Mol Cancer Res 7, 157-167 (2009).
16. Darnell, J. E., Jr. STATs and gene regulation. Science 277, 1630-1635 (1997).
17. Aggarwal, B. B. et al. Signal transducer and activator of transcription-3, inflammation, and cancer: how intimate is the relationship? Ann N Y Acad Sci 1171, 59-76 (2009).
18. Engelman, J. A., Luo, J. & Cantley, L. C. The evolution of phosphatidylinositol 3-kinases as regulators of growth and metabolism. Nat Rev Genet 7, 606-619 (2006).
19. Maehama, T. & Dixon, J. E. The tumor suppressor, PTEN/MMAC1, dephosphorylates the lipid second messenger, phosphatidylinositol 3,4,5-trisphosphate. J Biol Chem 273, 13375-13378 (1998).
20. Scheid, M. P. et al. Phosphatidylinositol (3,4,5)P3 is essential but not sufficient for protein kinase B (PKB) activation; phosphatidylinositol (3,4)P2 is required for PKB phosphorylation at Ser-473: studies using cells from SH2-containing inositol-5-phosphatase knockout mice. J Biol Chem 277, 9027-9035 (2002).
21. Vogt, P. K. & Hart, J. R. PI3K and STAT3: a new alliance. Cancer Discov 1, 481-486 (2011).
22. Rahaman, S. O. et al. Inhibition of constitutively active Stat3 suppresses proliferation and induces apoptosis in glioblastoma multiforme cells. Oncogene 21, 8404-8413 (2002).
23. Yang, J. et al. Stat3 activation is limiting for reprogramming to ground state pluripotency. Cell Stem Cell 7, 319-328 (2010).
24. Levy, D. E. & Darnell, J. E., Jr. Stats: transcriptional control and biological impact. Nat Rev Mol Cell Biol 3, 651-662 (2002).
25. Grivennikov, S. et al. IL-6 and Stat3 are required for survival of intestinal epithelial cells and development of colitis-associated cancer. Cancer Cell 15, 103-113 (2009).
26. de la Iglesia, N., Puram, S. V. & Bonni, A. STAT3 regulation of glioblastoma pathogenesis. Curr Mol Med 9, 580-590 (2009).
27. Sherry, M. M., Reeves, A., Wu, J. K. & Cochran, B. H. STAT3 is required for proliferation and maintenance of multipotency in glioblastoma stem cells. Stem Cells 27, 2383-2392 (2009).
28. Chung, C. D. et al. Specific inhibition of Stat3 signal transduction by PIAS3. Science 278, 1803-1805 (1997).
29. Veeriah, S. et al. The tyrosine phosphatase PTPRD is a tumor suppressor that is frequently inactivated and mutated in glioblastoma and other human cancers. Proc Natl Acad Sci USA 106, 9435-9440 (2009).
30. Jiang, X. et al. Activation of nonreceptor tyrosine kinase Bmx/Etk mediated by phosphoinositide 3-kinase, epidermal growth factor receptor, and ErbB3 in prostate cancer cells. J Biol Chem 282, 32689-32698 (2007).
31. Guryanova, O. A. et al. Nonreceptor tyrosine kinase BMX maintains self-renewal and tumorigenic potential of glioblastoma stem cells by activating STAT3. Cancer Cell 19, 498-511 (2011).
32. Zhang, T., Kee, W. H., Seow, K. T., Fung, W. & Cao, X. The coiled-coil domain of Stat3 is essential for its SH2 domain-mediated receptor binding and subsequent activation induced by epidermal growth factor and interleukin-6. Mol Cell Biol 20, 7132-7139 (2000).
33. Kim, E. et al. Phosphorylation of EZH2 activates STAT3 signaling via STAT3 methylation and promotes tumorigenicity of glioblastoma stem-like cells. Cancer Cell 23, 839-852 (2013).
34. Lee, J. et al. Tumor stem cells derived from glioblastomas cultured in bFGF and EGF more closely mirror the phenotype and genotype of primary tumors than do serum-cultured cell lines. Cancer Cell 9, 391-403 (2006).