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Standardized Cup Sizes
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Researchers zero in on estrogen's role in breast-cancer cell growth
Researchers zero in on estrogen's role in breast-cancer cell
growth
September 12, 2005
CHAMPAIGN, Ill.
- Why do estrogen-dependent breast-cancer cells
grow and spread rapidly? Researchers at the University of Illinois
at Urbana-Champaign say it may be because estrogen virtually
eliminates levels of a vitally important regulatory protein.
In a paper that will appear in the Sept. 13 issue of the
Proceedings of the National Academy of Sciences, the scientists
report that human breast-cancer cells exposed to estrogen in their
laboratory showed a dramatic reduction in numbers of a crucial
nuclear receptor corepressor, a protein known as N-CoR (pronounced
"en CORE"). They also found that the anti-estrogen drug tamoxifen,
often used in breast-cancer treatments, encouraged N-CoR recovery,
a beneficial activity.
The paper was published online last
week.
"Because estrogen has the ability to reduce the levels of N-CoR,
estrogen then can promote the proliferation and progression of
breast cancer, because the balance of co-activators and
co-repressors involved in normal gene transcription is altered,"
said Benita S. Katzenellenbogen, a Swanlund Professor of Cell and
Developmental Biology at Illinois. She also is a professor of
molecular and integrative physiology.
The findings may have sweeping implications, said
Katzenellenbogen and lead author Jonna Frasor, a postdoctoral
researcher who joins the faculty of the department of physiology
and biophysics in the U. of I. College of Medicine at Chicago this
month.
For one, the mechanisms at play could explain at least some of
the mixed results seen in women using estrogen and progesterone in
hormone therapy, said Katzenellenbogen, who also is a professor in
the U.
of I. College of Medicine at Urbana-Champaign.
While numbers of N-CoR proteins fell to 20 percent of normal,
the level of N-CoR's messenger RNA went untouched. The reduction of
N-CoR followed an up regulation of the ubiquitin ligase Siah2, an
enzyme that targets certain proteins for degradation, Frasor
said.
"Here we had an effect on the level of the N-CoR protein without
affecting the level of N-CoR mRNA," Katzenellenbogen said. "This is
the result of the initial effect of estrogen on gene expression,
which was to up regulate the mRNA levels for a ubiquitin ligase. So
by changing the level of this ligase, it had a dramatic effect on
the level of N-CoR protein without affecting gene expression for
N-CoR itself."
This "secondary effect" may have broad implications for other
important cellular activities, the researchers theorize.
Reductions
in N-CoR over time also could promote cancer development in other
sites, such as the uterus, and could adversely affect the desired
activities of vitamin D, retinoid and thyroid receptors,
Katzenellenbogen said.
The study sheds light on the impact of estrogen on certain
cells, as well as how tamoxifen works as an anti-estrogen to
facilitate recovery of N-CoR, she and Frasor said.
"Eventually," Katzenellenbogen said, "understanding more of the
mechanisms involved could lead to the development of other related
agents that might reduce some of the unwanted side effects of
tamoxifen, such as stimulation of the uterus."
In addition to Katzenellenbogen and Frasor, Jeanne M.
Danes, a
researcher in the department of molecular and integrative
physiology, and doctoral student Cory C. Funk were co-authors of
the study.
University of Illinois at Urbana-Champaign
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