A molecule found at high levels in cancer cells protects them from the
"cell-suicide" that is usually triggered by chemotherapy or radiation,
according to researchers at the University of Illinois at Chicago
College of Medicine.
The study, published online in the journal
PLoS One on Feb. 29,
suggests that two common cancer-fighting strategies may have "tremendous
synergy" if used in combination, says Andrei Gartel, UIC associate
professor of biochemistry and molecular genetics and medicine and
principal investigator on the study.
Damage to a cell's DNA can set in motion a cascade of signals that
triggers programmed cell death, or apoptosis. Radiation therapy and many
chemotherapy agents target and damage DNA somewhat selectively in
rapidly dividing cells, making them useful in fighting cancer. But many
cancer cells develop resistance over the course of treatment and block
the suicide pathway.
Based on the observation that a protein molecule in cancer cells called
FOXM1 is elevated following DNA damage, Gartel and his co-author sought
to investigate whether FOXM1 might have a role in protecting cancer
cells from apoptosis.
Using human cancer cells that were exposed to either chemicals or
radiation to damage DNA, the researchers used a variety of techniques to
decrease the levels of FOXM1 in these cells.
"We found a significant increase in DNA-damage-induced apoptosis in
cells with diminished levels of FOXM1," Gartel said. The results were
the same no matter what caused the DNA damage, or what method the
researchers used to reduce FOXM1.
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