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
相关论文
共 45 条
[1]   Molecular targets and anticancer potential of indole-3-carbinol and its derivatives [J].
Aggarwal, BB ;
Ichikawa, H .
CELL CYCLE, 2005, 4 (09) :1201-1215
[2]  
BLICK M, 1984, BLOOD, V64, P1234
[3]   Tissue distribution and quantitative analysis of estrogen receptor-alpha (ER alpha) and estrogen receptor-beta (ER beta) messenger ribonucleic acid in the wild-type and ER alpha-knockout mouse [J].
Couse, JF ;
Lindzey, J ;
Grandien, K ;
Gustafsson, JA ;
Korach, KS .
ENDOCRINOLOGY, 1997, 138 (11) :4613-4621
[4]   Estrogen receptors α and β:: Two receptors of a kind? [J].
Dechering, K ;
Boersma, C ;
Mosselman, S .
CURRENT MEDICINAL CHEMISTRY, 2000, 7 (05) :561-576
[5]   Mechanism of and requirement for estrogen-regulated MYB expression in estrogen-receptor-positive breast cancer cells [J].
Drabsch, Yvette ;
Hugo, Honor ;
Zhang, Rui ;
Dowhan, Dennis H. ;
Miao, Yu Rebecca ;
Gewirtz, Alan M. ;
Barry, Simon C. ;
Ramsay, Robert G. ;
Gonda, Thomas J. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (34) :13762-13767
[6]   The Dual, Opposing Roles of Estrogen in the Prostate [J].
Ellem, Stuart J. ;
Risbridger, Gail P. .
STEROID ENZYMES AND CANCER, 2009, 1155 :174-186
[7]   v-Myb of E26 leukemia virus up-regulates bcl-2 and suppresses apoptosis in myeloid cells [J].
Frampton, J ;
Ramqvist, T ;
Graf, T .
GENES & DEVELOPMENT, 1996, 10 (21) :2720-2731
[8]  
Funato T, 2001, ONCOL REP, V8, P807
[9]   The oestrogen receptors (ERα and ERβ) and their role in breast cancer:: a review [J].
Girdler, F ;
Brotherick, I .
BREAST, 2000, 9 (04) :194-200
[10]   Estrogen and MYB in breast cancer:: potential for new therapies [J].
Gonda, Thomas J. ;
Leo, Paul ;
Ramsay, Robert G. .
EXPERT OPINION ON BIOLOGICAL THERAPY, 2008, 8 (06) :713-717