A protein responsible for repairing damaged DNA may be a vital link to
explaining how smoking causes lung cancer, US researchers reported on
Tuesday.
Lung cells exposed to cigarette smoke produce less of the protein, called
FANCD2, the team at Oregon Health & Science University Cancer Institute
reported.
Without FANCD2, damaged DNA can cause cells to proliferate out of control
instead of destroying themselves as normal cells do.
The study, published in the British Journal of Cancer, could lead to better
treatments for lung cancer, the leading cause of cancer death globally, the
researchers said.
"These findings show the important role FANCD2 plays in protecting lung
cells against cigarette smoke, and may explain why cigarette smoke is so
toxic to these cells," said Laura Hays, who worked on the study.
"Although there are probably other proteins involved in this process, we
know this is a key one because cells with very high levels of FANCD2 were
resistant to the toxic effects of the smoke," said Grover Bagby, who oversaw
the work.
Hays and colleagues created an artificial windpipe in the lab to study the
effects of cigarette smoke on cells.
FANCD2 had already been linked with cancer. It is part of a family of
proteins involved in an inherited condition called Fanconi anemia. People
with Fanconi anemia have low levels of the proteins and are more likely to
develop cancers at a young age.
"This interesting piece of science adds to our understanding of why smoking
is so deadly. Smoking is the single biggest preventable cause of cancer and
causes nine out of 10 cases of lung cancer," Lesley Walker, director of
cancer information at Cancer Research UK, said in a statement.
Source : China Daily
