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J. Biol. Chem., Vol. 276, Issue 26, 23763-23768, June 29, 2001
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From the Department of Oncology, Vincent T. Lombardi Cancer Center,
Georgetown University, Washington, D. C. 20007
Human breast tumorigenesis is promoted by the
estrogen receptor pathway, and nuclear receptor coactivators are
thought to participate in this process. Here we studied whether one of
these coactivators, AIB1 (amplified in
breast cancer 1), was rate-limiting for
hormone-dependent growth of human MCF-7 breast cancer
cells. We developed MCF-7 breast cancer cell lines in which the
expression of AIB1 can be modulated by regulatable ribozymes directed
against AIB1 mRNA. We found that depletion of endogenous AIB1
levels reduced steroid hormone signaling via the estrogen receptor
Ribozyme Targeting Demonstrates That the Nuclear Receptor
Coactivator AIB1 Is a Rate-limiting Factor for
Estrogen-dependent Growth of Human MCF-7 Breast Cancer
Cells*
or progesterone receptor 
on transiently transfected
reporter templates. Down-regulation of AIB1 levels in MCF-7 cells did
not affect estrogen-stimulated cell cycle progression but reduced
estrogen-mediated inhibition of apoptosis and cell growth. Finally,
upon reduction of endogenous AIB1 expression,
estrogen-dependent colony formation in soft agar and tumor
growth of MCF-7 cells in nude mice was decreased. From these findings
we conclude that, despite the presence of different estrogen receptor
coactivators in breast cancer cells, AIB1 exerts a rate-limiting role
for hormone-dependent human breast tumor growth.
*
This work was supported by Department of Defense Breast
Cancer Research Program Grant DAMD17-99-1-9203 (to A. T. R.).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: Dept. Of Oncology,
Vincent T. Lombardi Cancer Center, Research Bldg., E307, Georgetown University, 3970 Reservoir Rd., Washington, D. C. 20007. Tel.: 202-687-1479; Fax: 202-687-4821.
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