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Switch of transforming growth factor beta function from tumor suppression to stimulation in adenomatous polyposis

Hongmei Wang1, Moltira Promkan, Guangming Liu

  • 1Department of Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine and SimmonsCooper Cancer Institute, Springfield, IL 62794-9677, United States.

Cancer Letters
|September 9, 2008
PubMed

Insights

Transforming growth factor beta (TGFbeta) can suppress or promote colon cancer. APC levels determine TGFbeta

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Transforming growth factor beta (TGFbeta) exhibits dual roles in cancer, acting as both a tumor suppressor and promoter.
  • The precise mechanisms governing TGFbeta's tumor-promoting functions in colon carcinoma remain largely unknown.
  • Mutant adenomatous polyposis coli (APC) is expressed in human colon carcinoma cells (CBS and Moser).

Purpose of the Study:

  • To elucidate the mechanisms by which TGFbeta influences colon cancer progression.
  • To investigate the role of adenomatous polyposis coli (APC) expression levels in modulating TGFbeta's function.

Main Methods:

  • Utilized human colon carcinoma cell lines (CBS and Moser) expressing mutant APC.
  • Performed APC knockdown experiments to assess changes in TGFbeta signaling.
  • Assessed cellular invasion, anchorage-independent growth, and gene expression (E-cadherin, p21/Waf1, TCF transcriptional activity).

Main Results:

  • TGFbeta exhibited tumor-suppressive effects in cells with normal APC expression levels.
  • Knockdown of APC transformed TGFbeta's function to tumor promotion, enhancing cellular invasion and anchorage-independent growth.
  • APC knockdown abrogated TGFbeta-induced expression of E-cadherin and p21/Waf1, while stimulating beta-catenin/Wnt pathway activity.

Conclusions:

  • Adenomatous polyposis coli (APC) expression levels are critical determinants of TGFbeta's functional outcome in colon cancer.
  • Reduced APC levels enable TGFbeta to promote tumor progression through modulation of key signaling pathways and gene expression.

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