« Previous
Next »
Gastroenterology
Volume 138, Issue 3
, Pages 1189-1199.e2
, March 2010
NFAT-Induced Histone Acetylation Relay Switch Promotes c-Myc-Dependent Growth in Pancreatic Cancer Cells
References
- Complexity of the early genetic response to growth factors in mouse fibroblasts. Mol Cell Biol. 1988;8:2140–2148
- . Growth factor-responsive genes in fibroblasts. Cell Growth Differ. 1990;1:305–309
- . Regulators of G1 cyclin-dependent kinases and cancers. Cancer Metastasis Rev. 2003;22:435–449
- . A network of immediate early gene products propagates subtle differences in mitogen-activated protein kinase signal amplitude and duration. Mol Cell Biol. 2004;24:144–153
- E2F4/5 and p107 as Smad cofactors linking the TGF-β receptor to c-myc repression. Cell. 2002;110:19–32
- . A tale of early response genes. Biol Pharm Bull. 2004;27:606–612
- . Signal transduction and the Ets family of transcription factors. Oncogene. 2000;19:6503–6513
- . Facilitating replication under stress: an oncogenic function of MYC?. Nat Rev Cancer. 2009;9:441–444
- . MAPK signal specificity: the right place at the right time. Trends Biochem Sci. 2006;31:268–275
- . Ets proteins in biological control and cancer. J Cell Biochem. 2004;91:896–903
- . Regulation of life and death by the zinc finger transcription factor Egr-1. J Cell Physiol. 2002;193:287–292
- . AP-1 in mouse development and tumorigenesis. Oncogene. 2002;20:2401–2412
- . Myc's broad reach. Genes Dev. 2008;22:2755–2766
- . Biology and management of pancreatic cancer. Postgrad Med J. 2008;84:478–497
- Pancreatic cancer: basic and clinical aspects. Gastroenterology. 2005;128:1606–1625
- Overexpression of c-myc in pancreatic cancer caused by ectopic activation of NFATc1 and the Ca2+/calcineurin signaling pathway. EMBO J. 2006;25:3714–3724
- The tumor suppressor KLF11 mediates a novel mechanism in transforming growth factor β-induced growth inhibition that is inactivated in pancreatic cancer. Mol Cancer Res. 2006;4:861–872
- Signaling disrupts mSin3A binding to the Mad1-like Sin3-interacting domain of TIEG2, an Sp1-like repressor. EMBO J. 2002;21:2451–2460
- Chimeric green fluorescent protein-aequorin as bioluminescent Ca2+ reporters at the single-cell level. Proc Natl Acad Sci U S A. 2000;97:7260–7265
- . Glowing jellyfish, luminescence and a molecule called coelenterazine. Trends Biotechnol. 1999;17:477–481
- Ectopic expression of VAV1 reveals an unexpected role in pancreatic cancer tumorigenesis. Cancer Cell. 2005;7:39–49
- Ras-MAPK signal transduction pathway, cancer and chromatin remodeling. Biochem Cell Biol. 2005;83:1–14
- c-myc Is a downstream target of the Smad pathway. J Biol Chem. 2002;277:854–861
- . Transcription factors of the NFAT family: regulation and function. Annu Rev Immunol. 1997;15:707–747
- Structure and chemistry of the p300/CBP and Rtt109 histone acetyltransferases: implications for histone acetyltransferase evolution and function. Curr Opin Struct Biol. 2008;18:741–747
- . NFAT signaling: choreographing the social lives of cells. Cell. 2002;109:67–79
- . A constitutively active NFATc1 mutant induces a transformed phenotype in 3T3-L1 fibroblasts. J Biol Chem. 2003;278:17246–17254
- . An emerging role for Ca2+/calcineurin/NFAT signaling in cancerogenesis. Cell Cycle. 2007;6:16–19
- Dual roles for NFAT transcription factor genes as oncogenes and tumor suppressors. Mol Cell Biol. 2008;28:7168–7181
- The role of NFAT transcription factors in integrin-mediated carcinoma invasion. Nat Cell Biol. 2002;4:540–544
Conflicts of interest The authors disclose no conflicts.
Funding Supported by the Deutsche Forschungsgemeinschaft (DFG, SFB-TR17; to V.E., A.G., and J.M.) and the Max Eder program of the German Cancer Research Foundation (Deutsche Krebshilfe, 70-3022-El I; to V.E.) and by the Miles and Shirley Fiterman Center for Digestive Diseases, Division of Gastroenterology and Hepatology, Division of Oncology Research, Mayo Clinic Cancer Center, Mayo Clinic Pancreatic SPORE P50 CA102701 and CA136526 (to M.E.F.-Z.).
PII: S0016-5085(09)01942-8
doi: 10.1053/j.gastro.2009.10.045
© 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
« Previous
Next »
Gastroenterology
Volume 138, Issue 3
, Pages 1189-1199.e2
, March 2010

