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Cell division can be halted in multiple ways, with implications for cancer


Brown University researchers have found that there are multiple independent ways to stop cell division, a phenomenon that prevents the spread of genetic mutation, which can make cells cancerous. Results of this research, along with an accompanying editorial, were published in the current issue of the journal Molecular Cell.

The findings will be of interest to scientists who are developing new-generation drugs that target cancer at the molecular level, according to John Sedivy, principal investigator of the study and a professor in the Department of Molecular Biology, Cell Biology and Biochemistry.

“If you can trip a senescence pathway,” Sedivy said, “you’d have a pretty terrific drug.”

Cells – except for cancerous ones – cannot reproduce forever. When aging cells stop dividing, they become “senescent.” Scientists believe one factor that causes senescence is the length of a cell’s telomeres, or protective caps on the end of chromosomes. Every time chromosomes reproduce, telomeres get shorter. As telomeres dwindle, cell division stops altogether. Senescent cells do not function the way young cells do, and are believed to be associated with skin wrinkles, immune system problems and age-related diseases, including cancer.

A protein called p21 acts as the molecular switch that triggers telomere-initiated senescence. A substantial part of the work reported by Sedivy and his team focuses on details of the pathways that trip the p21 switch, which were found to be similar, but not identical, to cellular responses to DNA damage. It is well known that if DNA is damaged, cells recognize the defect and stop dividing – a critical safeguard against cancer. The finding that dysfunctional telomeres can trigger similar responses is an important insight.

But Sedivy and his team also discovered another molecular mechanism that triggers senescence.

By manipulating single human cells in their laboratory, the researchers discovered that a protein called p16 also prompts cells to shut down and stop dividing. The team found that p16 operates independently from telomeres.

Sedivy said that p16, p21 and the upstream components that regulate senescence switches would all make compelling subjects of study for pharmaceutical companies, biotech firms and other university researchers.

“When it comes to developing drugs, this information is gold,” he said. “Because it should be possible to develop therapeutics to manipulate these targets.”

From start to finish, the research took two years to complete. Scientists at the Lawrence Berkeley National Laboratory in Berkeley, California provided technical assistance. The National Institutes of Health funded the project.

Wendy Lawton | Brown University
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