Researchers Identify New Target Protein for Colon Cancer


Researchers from Boston University School of Medicine (BUSM) identified a new potential target protein that may provide new therapies for treatment.

Colon cancer is a cancer of colon or rectum, located at the digestive tract’s lower end. According to the American Cancer Society around 97,220 new cases of colon cancer are registered in the U.S, in 2108. Major symptoms of the disease include abdominal pain and change in bowel habits. Now, researchers BUSM identified a new potential target protein called c-Cbl that might help understand the causes of colon cancer in depth and provide new therapies for treatment. It was observed that colon cancer patients with high levels of c-Cbl lived longer than those with low c-Cbl. The c-Cbl levels were analyzed in tumors isolated from people with colon cancer. The data of c-Cbl levels divided the patients into two groups, high c-Cbl and low c-Cbl.

The researchers split two types of colon cancer cells into three groups each. The first group comprised of un-manipulated colon cancer cells, second group consisted increased expression of normal c-Cbl, and third group had increased expression of the “off” version of c-Cbl.  The off version of c-Cbl lacked ubiquitin ligase activity that enabled the cells to grow more tumors than those that were given the ‘on’ version. Tumors require blood vessels to grow and metastasize. The researched observed the effect of c-Cbl on blood vessel growth by using three experimental models. The first group was normal, second group was given the c-Cbl protein, and third group was given the “off” version.  It was evident that the model that was given the “off” version of c-Cbl grew more blood vessels. This reveals that the ubiquitin ligase activity of c-Cbl is preventing tumors from growing and reducing tumor’s ability to grow blood vessels. Furthermore, c-Cbl might improve the survival of patients with colon cancer. The research was published in the American Journal of Pathology on June 17, 2108.


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