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J. Biol. Chem., Vol. 275, Issue 37, 28371-28379, September 15, 2000
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From the Müllerian inhibiting substance (MIS), a
member of the transforming growth factor-
Müllerian Inhibiting Substance Inhibits Breast Cancer
Cell Growth through an NF
B-mediated Pathway*
,,,,,, and
Pediatric Surgical Research Laboratories,
Massachusetts General Hospital and Harvard Medical School, Boston,
Massachusetts 02114, the § Department of Oncology, Queen's
University, Belfast BT9 7AB, Northern Ireland, and the
¶ Department of Radiation Medicine, Georgetown University Medical
Center, Washington, D. C. 20057
superfamily,
induces regression of the Müllerian duct in male embryos. In this
report, we demonstrate MIS type II receptor expression in normal breast
tissue and in human breast cancer cell lines, breast fibroadenoma, and
ductal adenocarcinomas. MIS inhibited the growth of both estrogen
receptor (ER)-positive T47D and ER-negative MDA-MB-231 breast cancer
cell lines, suggesting a broader range of target tissues for MIS
action. Inhibition of growth was manifested by an increase in the
fraction of cells in the G1 phase of the cell cycle
and induction of apoptosis. Treatment of breast cancer cells with MIS
activated the NF
B pathway and selectively up-regulated the immediate
early gene IEX-1S, which, when overexpressed, inhibited breast cancer
cell growth. Dominant negative IB
expression ablated both
MIS-mediated induction of IEX-1S and inhibition of growth, indicating
that activation of the NFB signaling pathway was required for these
processes. These results identify the NFB-mediated signaling pathway
and a target gene for MIS action and suggest a putative role for the MIS ligand and its downstream interactors in the treatment of ER-positive as well as negative breast cancers.
*
This work was supported by Grant IRG-173H from the American
Cancer Society and a breast cancer research grant from the
Massachusetts Department of Public Health (and to S. M.), National
Institutes of Health NCI Training Grant in Cancer Biology T32 CA 71345 and Resident Research Award from the American College of Surgeons (both to D. L. S.), and Grants HD32112 and CA17393
from the National Institutes of Health, NICHD and NCI, respectively
(both to P. K. D.).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.
To whom correspondence should be addressed: Pediatric Surgical
Research Laboratories, WRN1024, Massachusetts General Hospital, 55 Fruit St., Boston, MA 02114. Tel.: 617-724-6552; Fax: 617-724-7221; E-mail: maheswaran@helix.mgh.harvard.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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