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A report in Nature Structural and Molecular Biology investigates the mechanism by which cancer cells stop their chromosome ends from becoming shorter.
In order to keep their fitness, all cells need to prevent their chromosome ends (telomeres) from reducing with each division. The shortening of telomeres might be implicated in the aging process. For cancer cells, which divide more frequently than normal cells, the maintenance of telomeres is even more critical. Some types of cancer cells do this by producing more of an enzyme called telomerase; others use an alternative pathway (called ALT), whereby their telomeres get recruited to specialized regions in the nucleus, called PML bodies. Hongtao Yu and Patrick Ryan Potts determined that telomeres go to PML bodies when the proteins that cap the telomeres are tagged with a small protein called SUMO. They also identified the proteins that tag the telomeres. In their absence, the telomeres in ALT cancer cell lines get shorter, and the cells eventually lose their ability to grow. This work reveals a mechanism used by several kinds of cancer cells to proliferate, and could also have relevance for the normal physiology of cells. However, since the proteins play an important role in normal cells, targeting them for cancer therapy may not be feasible. Author contact: Hongtao Yu (University of Texas Southwestern Medical Center, Dallas, TX, USA)
E-mail: hongtao.yu@utsouthwestern.edu Abstract available online. (C) Nature Structural and Molecular Biology press release.
Message posted by: Trevor M. D'Souza
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