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Potential New Colorectal Cancer Treatment Target Identified

Last Updated: October 05, 2012.

 

Cell surface marker CD66c is novel marker that, when blocked, halts tumor growth in vivo

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The cell surface marker carcinoembryonic antigen-related cell adhesion molecule 6 is a novel marker for colorectal cancer stem cell isolation, which halts tumor growth when silenced, according to research published online Oct. 1 in Cancer.

FRIDAY, Oct. 5 (HealthDay News) -- The cell surface marker carcinoembryonic antigen-related cell adhesion molecule 6 (CD66c) is a novel marker for colorectal cancer stem cell isolation, which halts tumor growth when silenced, according to research published online Oct. 1 in Cancer.

Marica Gemei, Ph.D., of CEINGE-Advanced Biotechnology in Naples, Italy, and colleagues characterized CD66c expression in colorectal cancer stem cells by flow cytometry and immunohistochemistry in colon cancer samples and normal tissue. They evaluated its expression in colon cancer stem cells and in stem cell-enriched colon spheres and examined the role of RNA-mediated CD66c silencing on the in vitro and in vivo growth of Caco2 colon cancer cells.

Compared with normal colon tissues, the researchers found that CD66c expression was significantly higher in colorectal cancer samples, with expression correlating with cancer stage. Its expression was absent in Prominin 1 (CD133)-positive cells from normal colon but was brightest (CD66cbright) in CD133-positive colon cancer samples. In vitro experiments in stem cell-enriched colon spheres exhibited cells expressing CD66cbright, similar to that observed in fresh liver metastases. In Caco2 cells, CD66c silencing hampered in vitro proliferation and clonogenic potential, and in vivo xenograft experimentation attenuated the tumorigenic potential of Caco2 cells.

"CD66cbright expression was associated with colon cancer stem cells and CD66c silencing blocked tumor growth, thereby opening the way to a potential new treatment for colon cancer," the authors write.

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Copyright © 2012 HealthDay. All rights reserved.


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