Biology researchers at Rutgers-Newark have identified a new link between a specific protein and its role in determining how cancerous cells divide, spread and form new tumors in other parts of the human body.
In the article, “Rho Overexpression Leads to Mitosis-associated Detachment of Cells from Epithelial Sheets: A Link to the Mechanism of Cancer Dissemination,” appearing in the Aug. 9-13 edition of the Proceedings of the National Academy of Science, Rutgers-Newark Biology Chair Edward Bonder reveals that the overexpression of Rho protein in certain cells can cause the cells to take on a rounded shape, bud, break off and form cell colonies distant to the original cell colony.
By connecting the presence of Rho proteins to this cell division and movement phenomenon, researchers may have begun to pave the way for the development of more specific approaches to treat cancerous cells. For example, chemotherapy agents act to eradicate any cell that is dividing. With this approach, healthy cells are destroyed along with unhealthy ones, leading to the debilitating side effects experienced by many chemotherapy patients. Through the identification of the novel effect of a Rho pathway within a dividing cell, researchers may be able to develop more targeted pharmacological approaches that can attack unhealthy dividing cells while leaving the healthy ones intact.
Rho proteins serve as a regulator with the ability to turn on or activate other proteins, including myosin II, a motor protein instrumental in taking energy and converting it to movement in the human body. The researchers’ findings identified a link between cell division and a cell’s ability to remain associated with its parent tissue.
According to Bonder, researchers uncovered this information while attempting to learn more about what regulates the changes of cells within healing wounds in epithelial (skin) cells. After introducing Rho into a culture of cells, some cells budded out of the tissue monolayer after which they would get moved lengthy distances away from the original source of the cells.
“These cells continued to bud off rounded cells and they would remain loosely attached to the initial tissue monolayer,” Bonder explains. “We found that the rounded cells didn’t attach well to each other or to the cells in the original monolayer. Once they detached from the monolayer, they would float off and create another colony of cells at a distant location.” Bonder adds, “The observations help us define cross-talk between two different cytoskeletal elements. If you are able to define this, you can envision developing different pharmacological approaches to treat the spread of certain cancers. You can introduce agents that have a specific effect on this particular Rho pathway instead of knocking out all cells that are dividing.”