Identifying the molecular pathways that lead normal colon cells to become cancer cell could provide much needed biomarkers and therapeutic targets. Previously, , assistant professor of surgery, and colleagues showed that claudin-1鈥攁 protein member of 鈥渢ight junctions鈥� that help bind cells together into an organized tissue structure鈥攚as greatly increased and mislocalized in colorectal cancer.
In a recent report in , they describe the cellular pathway by which claudin-1 influences the transition of normal colon cells into cancerous ones. They show that increased claudin-1 expression in colon cancer cells is associated with loss of expression of the epithelial cell marker E-cadherin, whose reduced expression is correlated with poor prognosis and survival in colon cancer patients. Cell experiments showed that claudin-1 modulates expression of another protein, ZEB-1, which in turn affects E-cadherin expression. This chain of events then leads to cellular changes associated with invasion and progression in colon cancer cells.
The results suggest that ZEB-1, E-cadherin and claudin-1 could serve as biomarkers to indicate invasiveness and prognosis in colorectal cancer.
The research was supported by grants from the and the .