There were talks that the ALDH1B1 enzyme could be used as a potential marker for colon cancer. Now, researchers from the Vanderbilt-Ingram Cancer Center and the Vanderbilt Eye Institute reveal that the protein, blood vessel endocardial substance (BVES) which also plays a role in corneal cells may be a therapeutic target for ceasing the metastasis of colon cancer.
The findings also suggest a possible contribution of BVES in several epithelial cancers. This analysis essentially aims to halt the metastasis process which usually takes place when the epithelial cells go back to a less differentiated condition known as epithelial-mesenchymal transition (EMT).
Min Chang, M.D., an assistant professor of Ophthalmology and Visual Sciences and co-author on the study, specified, “When BVES is disrupted in corneal cells, they become disorganized, almost ‘cancer-like’.”
This sounds similar to cancer cells that expand their terrain, so the investigators looked for BVES-dependent phenotypes in cancer. When they inspected BVES expression in human colorectal cancers, they seemingly found very low proportions of BVES in many kinds of epithelial cancers like breast too.
While determining why BVES levels were so low, they uncovered that the BVES promoter was severely altered in such tumors, which seemed to cease its expression. In cellular trials, the team found that exposing the cells to a demethylating agent re-established the gene expression. BVES expression in colorectal cancer cell lines apparently resulted in them turning epithelial in nature and the tumor-like attributes also supposedly reduced.
Boosting levels of BVES could pave the path to reduced aggression of colorectal and other epithelial cancers. Scientists believe that it is not the initial tumor that is fatal but the metastatic pathway is what is considered dangerous.
The study is published in the October issue of the Journal of Clinical Investigation.