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Salk Institute scientists studying the relationship of telomeres to cancer made a surprising discovery: a cellular recycling process called autophagy -- generally thought of as a survival mechanism -- actually promotes the death of cells, thereby preventing cancer initiation.
The work, which appeared in the journal Nature on January 23, 2019, reveals autophagy to be a completely novel tumor-suppressing pathway and suggests that treatments to block the process in an effort to curb cancer may unintentionally promote it very early on.
Results - Surprise - Jan - Karlseder - Professor
"These results were a complete surprise," says Jan Karlseder, a professor in Salk's Molecular and Cell Biology Laboratory and the senior author of the paper. "There are many checkpoints that prevent cells from dividing out of control and becoming cancerous, but we did not expect autophagy to be one of them."
Each time cells duplicate their DNA to divide and grow, their telomeres get a little bit shorter. Once telomeres become so short that they can no longer effectively protect chromosomes, cells get a signal to stop dividing permanently. But occasionally, due to cancer-causing viruses or other factors, cells don't get the message and keep on dividing. With dangerously short or missing telomeres, cells enter a state called crisis, in which the unprotected chromosomes can fuse and become dysfunctional -- a hallmark of some cancers.
Karlseder - Team - Crisis - Crisis - Results
Karlseder's team wanted to better understand crisis -- both because crisis often results in widespread cell death that prevents precancerous cells from continuing to full-blown cancer and because the mechanism underlying this beneficial cell death isn't well-understood.
"Many researchers assumed cell death in crisis occurs through apoptosis, which along with autophagy is one of two types of programmed cell death," says Joe Nassour, a postdoctoral fellow in the Karlseder lab and the paper's first author. "But no one was doing experiments to find out if that was really the...
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