The mitogen-activated protein kinase pathway mediates growth arrest or E1A-dependent apoptosis in SKBr3 human breast cancer cells

International Journal of Cancer

Volumn 78, Issue 4, 1998, Pages 511-517

  Blagosklonny, Mikhail V ^a  

^a NATIONAL CANCER INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

MITOGEN ACTIVATED PROTEIN KINASE;

ANTINEOPLASTIC ACTIVITY; APOPTOSIS; ARTICLE; BREAST CANCER; CANCER INHIBITION; CELL PROLIFERATION; ENZYME ACTIVITY; HUMAN; HUMAN CELL; PRIORITY JOURNAL; SIGNAL TRANSDUCTION;

ADENOVIRUS E1A PROTEINS; APOPTOSIS; BREAST NEOPLASMS; CARCINOGENS; CELL CYCLE; CELL DIVISION; CYCLIN-DEPENDENT KINASE INHIBITOR P21; CYCLINS; ENZYME ACTIVATION; HUMANS; ISOENZYMES; PHORBOL ESTERS; PROTEIN KINASE C; PROTEIN KINASE C-ALPHA; PROTO-ONCOGENE PROTEINS C-RAF; RAS PROTEINS; TUMOR CELLS, CULTURED;

EID: 0031755805     PISSN: 00207136     EISSN: None     Source Type: Journal    
DOI: 10.1002/(SICI)1097-0215(19981109)78:4<511::AID-IJC19>3.0.CO;2-8     Document Type: Article

References (27)

1. AKTAS, H., CAI, H. and COOPER, G.M., Ras links growth factor signaling to the cell cycle machinery via regulation of cyclin D1 and the Cdk inhibitor p27KIP1. Mol. cell. Biol., 17, 3850-3857 (1997).
2. ALBLAS, J., SLAGER-DAVIDOV, R., STEENBERGH, P.H., SUSSENBACH, J.S. and VAN DER BURG, B., The role of MAP kinase in TPA-mediated cell cycle arrest of human breast cancer cells. Oncogene, 16, 131-139 (1998).
3. AN, W.G., SCHNUR, R.C., NECKERS, L.M. and BLAGOSKLONNY, M.V., Depletion of ErbB2, Raf-1 and mutant p53 proteins by geldanamycin derivatives correlates with antiproliterative activity. Cancer Chemother. Pharmacol., 40, 60-64 (1997).
4. BLAGOSKLONNY, M.V., ALVAREZ, M., FOJO, A. and NECKERS, L.M., Bcl-2 protein downregulation is not required for differentiation of multidrug resisitant HL60 leukemia cells, Leukemia Res., 20, 101-107 (1996).
5. BLAGOSKLONNY, M.V., GIANNAKAKOU, P., EL-DEIRY, W.S., KINGSTON, D.G.I., HIGGS, P.I., NECKERS, L.M. and FOJO, T., Raf1/bc12 phosphorylation: a step from microtubule damage to cell death. Cancer Res., 57, 130-135 (1997a).
6. BLAGOSKLONNY, M.V., PRABHU, N.S. and EL-DEIRY, W.S., Defects in p21WAF1/CIP1, Rb, c-myc signaling in phorbol ester-resistant cancer cells. Cancer Res., 57, 320-325 (1997b).
7. BLAGOSKLONNY, M.V., WU, G.S., SOMASUNDARAM, K. and EL-DEIRY, W.S., Wild-type p53 is not sufficient for serum starvation-induced apoptosis in cancer cells but accelerates apoptosis in sensitive cells. Int. J. Oncol., 11, 1165-1170 (1997c).
8. CANMAN, C.E., GILMER, T.M., COUTTS, S.B. and KASTAN, M.B., Growth factor modulation of p53-mediated growth arrest versus apoptosis. Genes Develop., 9, 600-611 (1995).
9. COWLEY, S., PETERSON, H., KEMP, P. and MARSHALL, C.J., Activation of MAP kinase kinase is necessary and sufficient for PC12 differentiation and for transformation of NIH 3T3 cells. Cell, 77, 841-852 (1994).
10. DATTO, M.B., HU, P.P., KOWALIK, T.F., YINGLING, J. and WANG, X.F., The viral oncoprotein E1A blocks transforming growth factor beta-mediated induction of p21/WAF1/CIP1 and p15/INK4B. Mol. cell. Biol., 17, 2030-2037 (1997).
11. 1 cyclin-dependent kinase activity. Genes Develop., 9, 2873-2887 (1995).
12. EL-ASHRY, D., MILLER, D.L., KHARBANDA, S., LIPPMAN, M.E. and KERN, F.G., Constitutive Raf-1 kinase activity in breast cancer cells induces both estrogen-independent growth and apoptosis. Oncogene, 15, 423-435 (1997).
13. HOWE, J.A., MYMRYK, J.S., EGAN, C., BRANTON, P.E. and BAYLEY, S.T., Retinoblastoma growth suppressor and a 300-kDa protein appear to regulate cellular DNA synthesis. Proc. nat. Acad. Sci. (Wash.), 87, 5883-5887 (1990).
14. 1 pathways. Proc. nat. Acad. Sci. (Wash.), 92, 4793-4797 (1995).
15. LIU, Y., MARTINDALE, J.L., GOROSPE, M. and HOLBROOK, N.J., Regulation of p21 WAF1/CIP1 expression through mitogen-activated protein kinase signaling pathway. Cancer Res., 56, 31-35 (1996).
16. MISSERO, C., CALAUTTI, E., ECKNER, R., CHIN, J., TSAI, L.H., LIVINGSTON, D.M. and DOTTO, G.P., Involvement of the cell-cycle inhibitor Cip1/WAF1 and the E1A-associated p300 protein in terminal differentiation; Proc. nat. Acad. Sci. (Wash.), 92, 5451-5455 (1995).
17. MYMRYK, J.S., SHIRE, K. and BAYLEY, ST., Induction of apoptosis by adenovirus type 5 E1A in rat cells requires a proliferative block. Oncogene, 9, 1187-1193 (1994).
18. PUMIGLIA, K.M. and DECKER, S.J., Cell cycle arrest mediated by the MEK/mitogen-activated protein kinase pathway. Proc. nat. Acad. Sci. (Wash.), 94, 448-452 (1997).
19. SCHULTE, T.W., BLAGOSKLONNY, M.V., ROMANOVA, L., MUSHINSKI, J.F., MONIA, B.P., JOHNSTON, J.F., NGUYEN, P., TREPEL, J. and NECKERS, L.M., Destabilization of Raf-1 by geldanamycin leads to disruption of the Raf-1-MEK-mitogen-activated protein kinase signalling pathway. Mol. Cell. Biol. 16, 5839-5845 (1996).
20. SCHWALLER, J., PETERS, U.R., PABST, T., NIKLAUS, G., MACFARLANE, D.E., FEY, M.F. and TOBLER, A., Up-regulation of p21WAF1 expression in myeloid cells is activated by the protein kinase C pathway. Brit. J. Cancer, 76, 1554-1557 (1997).
21. SEGER, R. and KREBS, E.G., The MAPK signaling cascade. FASEB J., 9, 726-735. (1995).
22. SEWING, A., WISEMAN, B., LLOYD, A.C. and LAND, H., High-intensity Raf signal causes cell cycle arrest mediated by p21Cip1. Mol. cell. Biol., 17, 5588-5597 (1997).
23. WEINBERG, R.A., The retinobiastoma protein and cell cycle control. Cell, 81, 323-330 (1995).
24. WOODS, D., PARRY, D., CHERWINSKI, H., BOSCH, E., LEES, E. and MCMAHON, M., Raf-induced proliferation or cell cycle arrest is determined by the level of Raf activity with arrest mediated by p21Cip1. Mol. cell. Biol., 17, 5598-5611 (1997).
25. ZENG, Y.X. and EL-DEIRY, W.S., Regulation of p21WAF1/CIP1 expression by p53-independent pathways. Oncogene, 12, 1557-1565 (1996).
26. ZHANG, H., HANNON, G.J. and BEACH, D., p21-containing cyclin kinases exist in both active and inactive states. Genes Develop., 8, 1750-1758 (1994).
27. ZOU, X., RUDCHENKO, S., WONG, K. and CALAME, K., Induction of c-myc transcription by the v-Abl tyrosine kinase requires Ras, Raf1, and cyclin-dependent kinases. Genes Develop., 11, 654-662 (1997).