Tumor Biology

, Volume 31, Issue 1, pp 16–22

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


    • Department of Natural SciencesAssumption College
  • Kristin Doucet
    • Department of Natural SciencesAssumption College
  • Victoria Duke
    • Department of Natural SciencesAssumption College
  • Amber Morra
    • Department of Natural SciencesAssumption College
  • Nicole Johnson
    • Department of Natural SciencesAssumption College
Research Article

DOI: 10.1007/s13277-009-0003-2

Cite this article as:
Wilkins, H.R., Doucet, K., Duke, V. et al. Tumor Biol. (2010) 31: 16. doi:10.1007/s13277-009-0003-2


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 beta-estradiol 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 β-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.



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© International Society of Oncology and BioMarkers (ISOBM) 2009