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J Biol Chem, Vol. 273, Issue 47, 31308-31316, November 20, 1998
From the Department of Medicine, Campus Box B151, University of
Colorado Health Sciences Center, Denver, Colorado 80262
During late stages of breast cancer progression,
tumors frequently acquire steroid hormone resistance with concurrent
amplification of growth factor receptors; this alteration predicts a
poor prognosis. We show here that following treatment with the
progestin, R5020, breast cancer cells undergo a "biochemical shift"
in the regulation of epidermal growth factor (EGF)-stimulated signaling
pathways: R5020 potentiates the effects of EGF by up-regulating EGFR,
c-ErbB2 and c-ErbB3 receptors, and by enhancing EGF-stimulated tyrosine phosphorylation of signaling molecules known to associate with activated type I receptors. Independently of EGF, R5020 increases Stat5
protein levels, association of Stat5 with phosphotyrosine-containing proteins, and tyrosine phosphorylation of JAK2 and Shc. Furthermore, progestins "prime" breast cancer cells for growth signals by
potentiating EGF-stimulated p42/p44 mitogen-activated protein kinase
(MAPK), p38 MAP kinase, and JNK activities. Although the levels of
cyclin D1, cyclin E, and p21WAF1, are up-regulated by
R5020 alone, they are synergistically up-regulated by EGF in the
presence of R5020. Up-regulation of cell cycle proteins by EGF is
blocked by inhibition of p42/p44 MAPK only in the presence of R5020,
supporting a shift in the regulation of these cell cycle mediators from
MAPK-independent to MAPK-dependent pathways. In summary,
progesterone selectively increases the sensitivity of key kinase
cascades to growth factors, thereby priming cells for stimulation by
latent growth signals. These data support a model in which breast
cancer cell growth switches from steroid hormone to growth factor dependence.
Convergence of Progesterone and Epidermal Growth Factor Signaling
in Breast Cancer
POTENTIATION OF MITOGEN-ACTIVATED PROTEIN KINASE PATHWAYS
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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H. Matsuura, M. Sakaue, K. Subbaramaiah, H. Kamitani, T. E. Eling, A. J. Dannenberg, T. Tanabe, H. Inoue, J. Arata, and A. M. Jetten Regulation of Cyclooxygenase-2 by Interferon gamma and Transforming Growth Factor alpha in Normal Human Epidermal Keratinocytes and Squamous Carcinoma Cells. ROLE OF MITOGEN-ACTIVATED PROTEIN KINASES J. Biol. Chem., October 8, 1999; 274(41): 29138 - 29148. [Abstract] [Full Text] [PDF]
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