Estrogen prevents sustained COLO-205 human colon cancer cell growth by inducing apoptosis, decreasing c-myb protein, and decreasing transcription of the anti-apoptotic protein bcl-2

被引:41
|
作者
Wilkins, Heather R. [1 ]
Doucet, Kristin [1 ]
Duke, Victoria [1 ]
Morra, Amber [1 ]
Johnson, Nicole [1 ]
机构
[1] Assumption Coll, Dept Nat Sci, Worcester, MA 01609 USA
关键词
c-myb; Estrogen; COLO-205; bcl-2; Apoptosis; HORMONE REPLACEMENT THERAPY; BREAST-CANCER; RECEPTOR-BETA; COLORECTAL-CANCER; ER-BETA; SIGNAL-TRANSDUCTION; EXPRESSION; ALPHA; PROLIFERATION; PROTOONCOGENE;
D O I
10.1007/s13277-009-0003-2
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The proto-oncogene c-myb is overexpressed in human colon cancer cells. c-myb is known to be affected by estrogen in some breast cancers and leukemias. However, the mechanism of c-myb regulation via estrogen in colon cancer requires further investigation. Human COLO-205 colon cancer cells were cultured and treated with betaestradiol for 24 h. Apoptosis was quantified using acridine orange/propidium iodide labeling and confirmed with DNA fragmentation gel electrophoresis. Expression of c-myb protein was assessed via SDS-PAGE and immunoblotting and RT-PCR was used to quantify bcl-2 RNA. Protein and RNA expression levels were also assayed after c-myb siRNA treatment for 24 h. We demonstrate an increase in apoptosis after 24 h of beta-estradiol treatment of human COLO-205 colon cancer cells. Estrogen treatment also decreases c-myb protein levels as well as expression of its transcriptional target bcl-2. Suppression of c-myb protein also results in increased apoptosis and decreases bcl-2 expression. These results indicate that estrogen has a protective effect from sustained colon cancer cell growth at least partly through suppression of c-myb and bcl-2.
引用
收藏
页码:16 / 22
页数:7
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