Protection from rapamycin-induced apoptosis by insulin-like growth factor-I is partially dependent on protein kinase C signaling

Cancer Research

Volumn 70, Issue 5, 2010, Pages 2000-2009

  Thimmaiah, Kuntebommanahalli N ^a   Easton, John B ^a   Houghton, Peter J ^b  

^a ST JUDE CHILDREN S RESEARCH HOSPITAL   (United States)

^b NATIONWIDE CHILDREN S HOSPITAL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

2 (2 AMINO 3 METHOXYPHENYL)CHROMONE; ALANINE; CALPHOSTIN C; MITOGEN ACTIVATED PROTEIN KINASE 1; MITOGEN ACTIVATED PROTEIN KINASE 3; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN BAD; PROTEIN BID; PROTEIN KINASE B BETA; PROTEIN KINASE C; PROTEIN KINASE C EPSILON; PROTEIN KINASE C MU; PROTEIN KINASE C THETA; PROTEIN P90; RAPAMYCIN; SERINE; SMALL INTERFERING RNA; SOMATOMEDIN C; WORTMANNIN;

APOPTOSIS; ARTICLE; CELL DEATH; CONTROLLED STUDY; CYTOSOL; ENZYME PHOSPHORYLATION; HUMAN; HUMAN CELL; IMMUNOPRECIPITATION; MITOCHONDRION; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; SARCOMA CELL;

1-PHOSPHATIDYLINOSITOL 3-KINASE; 14-3-3 PROTEINS; APOPTOSIS; BCL-ASSOCIATED DEATH PROTEIN; CELL LINE, TUMOR; CYCLIC AMP-DEPENDENT PROTEIN KINASES; EPIDERMAL GROWTH FACTOR; HUMANS; INSULIN; INSULIN-LIKE GROWTH FACTOR I; INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS; MITOGEN-ACTIVATED PROTEIN KINASE 1; MITOGEN-ACTIVATED PROTEIN KINASE 3; PHOSPHORYLATION; PLATELET-DERIVED GROWTH FACTOR; PROTEIN KINASE C; PROTEIN-SERINE-THREONINE KINASES; PROTO-ONCOGENE PROTEINS C-BCL-2; RHABDOMYOSARCOMA; SIROLIMUS;

EID: 77950262746     PISSN: 00085472     EISSN: 15387445     Source Type: Journal    
DOI: 10.1158/0008-5472.CAN-09-3693     Document Type: Article

References (37)

1. Yang E, Zha J, Jockel J, Boise LH, Thompson CB, Korsmeyer SJ. Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death. Cell 1995;80:285-291
2. Zha J, Harada H, Yang E, Jockel J, Korsmeyer SJ. Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L). Cell 1996;87:619-628
3. Zha J, Harada H, Osipov K, Jockel J, Waksman G, Korsmeyer SJ. BH3 domain of BAD is required for heterodimerization with BCL-XL and pro-apoptotic activity. J Biol Chem 1997;272:24101-24104
4. Alessi DR, Cuenda A, Cohen P, Dudley DT, Saltiel AR. PD 098059 is a specific inhibitor of the activation of mitogen-activated protein kinase kinase in vitro and in vivo. J Biol Chem 1995;270:27489-27494
5. Harada H, Andersen JS, Mann M, Terada N, Korsmeyer SJ. p70S6 kinase signals cell survival as well as growth, inactivating the pro-apoptotic molecule BAD. Proc Natl Acad Sci U S A 2001;98:9666-9670
6. Datta SR, Dudek H, Tao X, et al. Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery. Cell 1997;91:231-241
7. Harada H, Becknell B, Wilm M, et al. Phosphorylation and inactivation of BAD by mitochondria-anchored protein kinase A. Mol Cell 1999;3:413-422
8. Schurmann A, Mooney AF, Sanders LC, et al. p21-activated kinase 1 phosphorylates the death agonist bad and protects cells from apoptosis. Mol Cell Biol 2000;20:453-461
9. Shimamura A, Ballif BA, Richards SA, Blenis J. Rsk1 mediates a MEK-MAP kinase cell survival signal. Curr Biol 2000;10:127-135
10. Tan Y, Ruan H, Demeter MR, Comb MJ. p90(RSK) blocks bad-mediated cell death via a protein kinase C-dependent pathway. J Biol Chem 1999;274:34859-34867
11. Dramsi S, Scheid MP, Maiti A, et al. Identification of a novel phosphorylation site, Ser-170, as a regulator of bad pro-apoptotic activity. J Biol Chem 2002;277:6399-6405
12. Konishi Y, Lehtinen M, Donovan N, Bonni A. Cdc2 phosphorylation of BAD links the cell cycle to the cell death machinery. Mol Cell 2002;9:1005-1016
13. Deng H, Yu F, Chen J, Zhao Y, Xiang J, Lin A. Phosphorylation of Bad at Thr-201 by JNK1 promotes glycolysis through activation of phosphofructokinase-1. J Biol Chem 2008;283:20754-20760
14. Willis SN, Fletcher JI, Kaufmann T, et al. Apoptosis initiated when BH3 ligands engage multiple Bcl-2 homologs, not Bax or Bak. Science 2007;315:856-859
15. Maslyar DJ, Aoki M, Vogt PK. The growth-promoting activity of the Bad protein in chicken embryo fibroblasts requires binding to protein 14-3-3. Oncogene 2001;20:5087-5092
16. Chattopadhyay A, Chiang CW, Yang E. BAD/BCL-[X(L)] heterodimerization leads to bypass of G0/G1 arrest. Oncogene 2001;20:4507-4518
17. Masters SC, Subramanian RR, Truong A, et al. Survival-promoting functions of 14-3-3 proteins. Biochem Soc Trans 2002;30:360-365
18. Thimmaiah KN, Easton J, Huang S, et al. Insulin-like growth factor Imediated protection from rapamycin-induced apoptosis is independent of Ras-Erk1-2 and phosphatidylinositol 3′-kinase-Akt signaling pathways. Cancer Res 2003;63:364-374
19. Kurmasheva RT, Dudkin L, Billups C, Debelenko LV, Morton CL, Houghton PJ. The insulin-like growth factor-1 receptor-targeting antibody, CP-751,871, suppresses tumor-derived VEGF and synergizes with rapamycin in models of childhood sarcoma. Cancer Res 2009;69:7662-7671
20. Hosoi H, Dilling MB, Shikata T, et al. Rapamycin causes poorly reversible inhibition of mTOR and induces p53-independent apoptosis in human rhabdomyosarcoma cells. Cancer Res 1999;59:886-894
21. Roberts ML, Virdee K, Sampson CP, Gordon I, Parone P, Tolkovsky AM. The combination of bcl-2 expression and NGF-deprivation facilitates the selective destruction of BAD protein in living sympathetic neurons. Mol Cell Neurosci 2000;16:97-110.
22. Zhou XM, Liu Y, Payne G, Lutz RJ, Chittenden T. Growth factors inactivate the cell death promoter BAD by phosphorylation of its BH3 domain on Ser155. J Biol Chem 2000;275:25046-25051
23. Virdee K, Parone PA, Tolkovsky AM. Phosphorylation of the proapoptotic protein BAD on serine 155, a novel site, contributes to cell survival. Curr Biol 2000;10:R883.
24. Tan Y, Demeter MR, Ruan H, Comb MJ. BAD Ser-155 phosphorylation regulates BAD/Bcl-XL interaction and cell survival. J Biol Chem 2000;275:25865-25869
25. Lizcano JM, Morrice N, Cohen P. Regulation of BAD by cAMPdependent protein kinase is mediated via phosphorylation of a novel site, Ser155. Biochem J 2000;349:547-557
26. Datta SR, Katsov A, Hu L, et al. 14-3-3 proteins and survival kinases cooperate to inactivate BAD by BH3 domain phosphorylation. Mol Cell 2000;6:41-51.
27. Yao R, Cooper GM. Growth factor-dependent survival of rodent fibroblasts requires phosphatidylinositol 3-kinase but is independent of pp70S6K activity. Oncogene 1996;13:343-351
28. Vemuri GS, McMorris FA. Oligodendrocytes and their precursors require phosphatidylinositol 3-kinase signaling for survival. Development 1996;122:2529-2537
29. Scheid MP, Lauener RW, Duronio V. Role of phosphatidylinositol 3-OH-kinase activity in the inhibition of apoptosis in haemopoietic cells: phosphatidylinositol 3-OH-kinase inhibitors reveal a difference in signalling between interleukin-3 and granulocyte-macrophage colony stimulating factor. Biochem J 1995;312:159-162
30. Datta K, Bellacosa A, Chan TO, Tsichlis PN. Akt is a direct target of the phosphatidylinositol 3-kinase. Activation by growth factors, v-src and v-Ha-ras, in Sf9 and mammalian cells. J Biol Chem 1996;271:30835-30839
31. Dudek H, Datta SR, Franke TF, et al. Regulation of neuronal survival by the serine-threonine protein kinase Akt. Science 1997;275:661-665
32. O'Shea C, Klupsch K, Choi S, et al. Adenoviral proteins mimic nutrient/ growth signals to activate the mTOR pathway for viral replication. EMBO J 2005;24:1211-1221
33. Jin Z, Xin M, Deng X. Survival function of protein kinase Cι as a novel nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-activated bad kinase. J Biol Chem 2005;280:16045-16052
34. Villalba M, Bushway P, Altman A. Protein kinase C-theta mediates a selective T cell survival signal via phosphorylation of BAD. J Immunol 2001;166:5955-5963
35. Aitken A. 14-3-3 and its possible role in co-ordinating multiple signalling pathways. Trends Cell Biol 1996;6:341-347
36. Wang SW, Denny TA, Steinbrecher UP, Duronio V. Phosphorylation of Bad is not essential for PKB-mediated survival signaling in hemopoietic cells. Apoptosis 2005;10:341-348
37. Vogel A, Aslan JE, Willenbring H, et al. Sustained phosphorylation of Bid is a marker for resistance to Fas-induced apoptosis during chronic liver diseases. Gastroenterology 2006;130:104-119