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BVES butts heads with colorectal cancer

JCI Journals

Once a cancer gains the ability to invade local tissues and spread to a distant site it becomes much harder to treat. A team of researchers, led by Min Chang and Christopher Williams, at Vanderbilt University School of Medicine, Nashville, has now identified the protein BVES as a suppressor of colorectal cancer progression to this dangerous state, leading them to suggest that BVES could be a therapeutic or preventative target in colorectal cancer.

Cancers originating from cells covering any of the external and internal surfaces of the body (epithelial cells) are known as epithelial cancers. If such cancers (e.g., colorectal cancer) are to become invasive and spread to distant sites in the body, some of the epithelial cancer cells must acquire the characteristics of a different cell type, a mesenchymal cell. Protein complexes that link epithelial cells together (junctional complexes) are regulators of epithelial-mesenchymal transition (EMT). Chang, Williams, and colleagues found that the junctional protein BVES regulates EMT in human colon cancer cells. Importantly, the team found that BVES expression was reduced in all stages of human colorectal carcinoma and that restoring BVES expression to normal decreased the in vitro and in vivo cancer cell characteristics of human colon cancer cells. These data provide the rational for the suggestion that targeting BVES could be of benefit to individuals with colorectal cancer.


TITLE: BVES regulates EMT in human corneal and colon cancer cells and is silenced via promoter methylation in human colorectal carcinoma

Min S. Chang
Vanderbilt Eye Institute, Nashville, Tennessee, USA.
Phone: 615.936.6413; Fax: 615.936.6410; E-mail:

Christopher S. Williams
Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Phone: 615.322.3642; Fax: 615.343.6229; E-mail:

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