Once these compounds arrest mitosis, cell death depends on competing signaling networks in each cell, according to paper in Cancer Cell.
Cell behavior as a result of antimitotic cancer drugs is more variable than previously recognized, according to scientists at the University of Manchester. They found that besides the various cell lines they used responding differently to these medications, cells within a cell line also demonstrated a range of reactions.
The team used a high-throughput, automated time-lapse light microscopy to analyze over 10,000 single cells from 15 cell lines in response to three different classes of antimitotic drug.
“We know that antimitotic drugs block the final stage of the cell division process, mitosis,” notes Stephen Taylor, Ph.D., University’s faculty of life sciences. “How the cells then die is a mystery.
“In essence, it turns out that when cells are exposed to these drugs they arrest in mitosis. Then a race starts between two competing cellular signaling networks. One network is trying to kill the cell, the other is trying to cause the cell to exit mitosis and thus allow the cell to survive. The factors influencing the race not only vary from cell line to cell line but also within cells from the same line, explaining why there is so much complexity,” Dr. Taylor explains.
“What we want to do now is figure out how we can help the cell death pathway win the race more often. This would hopefully mean that the anti-mitotic drugs would be better at killing cancer cells.
Dr. Taylor worked along with Karen Gascoigne, a graduate student. Their research appears in the August issue of Cancer Cell.
