Attacking Cancer By Attacking Telomerase

Cancers depend on continually lengthening telomeres to overcome limits on cell proliferation. If that process can be blocked, it would stop cancer in its tracks. This is the basis of the SENS approach to cancer, WILT, but there are other initiatives aimed at a similar goal: "It starts with the enzyme telomerase, which affects the caps, or telomeres, at the end of a chromosome. Telomeres shorten over time. But telomerase prevents this from happening, making the cell immortal. If cancer is triggered in the cell, the presence of telomerase leads to the growth of the cancer. Telomerase is kept in control by the protein TRF1, which keeps the telomeres operating correctly. But another protein, Fbx4, can bind to TRF1 and degrade it, causing the telomeres to lengthen. Now, researchers have discovered, a third protein, TIN2, can step in and override Fbx4 by binding to TRF1 first and preventing Fbx4 from attaching to it. This finding paves the way for developing a drug that acts like TIN2, keeping everything in check ... In 90 percent of cancers, no matter what caused the cancer to form, it needs telomerase activity to maintain the cell. Without telomerase, the cell will die. Our work is key to understanding a detailed mechanism for how these molecules interact and how to design a drug to block Fbx4."

Link: http://www.sciencedaily.com/releases/2010/02/100217074950.htm