According to a recent article in Fierce Biotech, most cancers progress through constant cell division. Scientists at Vanderbilt University are determined to find the reason for this mysterious cell division.
The Vanderbilt team found a genetic switch that appears to set off the abnormal amplification of cells. Again, CRISPR’s gene-editing mechanism was at the center of the discovery.
Focusing on the TRAF3 Gene
The scientists used a genome-wide CRISPR screen and found that when they deleted a protein that is produced by the TRAF3 gene, the cells proliferate non-stop. The spread of cells continued even though they reach a density that would generally cause them to stop dividing.
Noncancerous cells will stop dividing when they sense cell density but as aforementioned, cancer cells keep dividing.
The Team’s Critical Insights
The Vanderbilt team was quoted in the journal eLife that since TRAF3 had not been previously associated with cancer, their finding may suggest critical insights into how some cancers develop.
The Vanderbilt team’s investigation began with forty million epithelial cells which are cells lining and protecting an organ’s surface. CRISPR was used to identify epithelial cells that were dividing uncontrollably. The team confirmed that low expression of TRAF3 mutations is related to more severe outcomes.
They reported that the deletion of TRAF3 creates signaling that leads to cell proliferation. TRAF3 generally activates immunity and had not, in the past, been associated with the uncontrolled growth of cells.
Certain cancers that originate in epithelial tissues are lung and gastric cancers. Therefore, the team’s discovery that TRAF3 plays a role in cell division by using epithelial cells will be helpful in understanding other cancers.