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J. Biol. Chem., Vol. 275, Issue 43, 33937-33944, October 27, 2000
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From the Overexpression of the oncogene for ErbB-2 is an
unfavorable prognostic marker in human breast cancer. Its oncogenic
potential appears to depend on the state of tyrosine phosphorylation.
However, the mechanisms by which ErbB-2 is constitutively
tyrosine-phosphorylated in human breast cancer are poorly understood.
We now show that human breast carcinoma samples with ErbB-2
overexpression have higher proliferative and metastatic activity in the
presence of autocrine secretion of prolactin (PRL). By using a
neutralizing antibody or dominant negative (DN) strategies or specific
inhibitors, we also show that activation of Janus kinase Jak2 by
autocrine secretion of PRL is one of the significant components of
constitutive tyrosine phosphorylation of ErbB-2, its association with
Grb2 and activation of mitogen-activated protein (MAP) kinase in human breast cancer cell lines that overexpress ErbB-2. Furthermore, the
neutralizing anti-PRL antibody or erbB-2 antisense
oligonucleotide or DN Jak2 or Jak2 inhibitor or DNRas or MAP kinase
kinase inhibitor inhibits the proliferation of both untreated and
PRL-treated cells. Our results indicate that autocrine secretion of PRL
stimulates tyrosine phosphorylation of ErbB-2 by Jak2, provides docking
sites for Grb2 and stimulates Ras-MAP kinase cascade, thereby causing unrestricted cellular proliferation. The identification of this novel
cross-talk between ErbB-2 and the autocrine growth stimulatory loop for
PRL may provide new targets for therapeutic and preventive intervention
of human breast cancer.
Constitutive Tyrosine Phosphorylation of ErbB-2 via Jak2 by
Autocrine Secretion of Prolactin in Human Breast Cancer*
,,,,,,
,,,,, and¶¶
Department of Internal Medicine, Graduate
School of Medicine, University of Tokyo, Tokyo 113, the
§ Department of Pathology, Graduate School of Medicine,
University of Tokyo, Tokyo 113, the ¶ Department of Molecular
Pathogenesis, Nagoya University School of Medicine, Nagoya 466, the
Second Department of Internal Medicine, Tokyo Women's Medical
College, Tokyo 162, the ** Department of Oncology, Institute of Medical
Science, University of Tokyo, Tokyo 108, the
Department of Obstetrics and Gynecology,
Graduate School of Medicine, University of Tokyo, Tokyo 113, and the
§§ International Medical Center of Japan,
Tokyo 162, Japan
*
This work was supported by a grant from the Research
Fellowships of the Japan Society for the Promotion of Science for Young Scientists (to T. Y.), by health sciences research grants (for research on human genome and gene therapy) from the Ministry of Health
and Welfare (to T. K.), and by health sciences research grants
(for research on second term comprehensive 10-year strategy for cancer
control) from the Ministry of Health and Welfare (to Y. Y.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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