Colon cancer, also considered as colorectal cancer or bowel cancer, is the cancer of the epithelial cells lining the colon. There are many risk factors and many prophylactic measurements against this cancer. 95% of colon cancer is known as adenocarcinoma, mainly divided into different stages according to invasiveness and metastatic ability of the tumor. Many mutations are acquired, leading to this malignancy. Mainly, these occur in entities that greatly alter and affect the cell cycle, cell signaling pathways, cell movement, which all involve the action of Rho GTPases. The protein of our interest is DLC2, also known as StarD13 or START-GAP2, a GAP for Rho and Cdc42. Literature states that this protein is considered a tumor-suppressor in hepatocellular carcinoma. Previous work in our lab proved StarD13 to be a tumor suppressor in brain tumor and in breast cancer. In this work, we studied the role of StarD13 in colon cancer.
When overexpressed, StarD13 led to a decrease in cell proliferation in colon cancer cells. This was measured by WST MTT kits. Knocking down StarD13 using StarD13 siRNA led to an increase in cell proliferation. This showed that, similarly to its role in astrocytoma and breast cancer, StarD13 seems to be a tumor suppressor in colon cancer as well. We were also interested in examining the role of StarD13 in cell motility. StarD13 knock down resulted in an inhibition of cell motility, as seen by time lapse microscopy. This might be due to the inhibition of Rho, thus Rac-dependant focal complexes are not formed nor detached for the cells to move forward. future work is still needed to determine the exact mechanism of inhibition.