According to a new study in Science Translational Medicine, a protein called Rac1b may be the key actor in the "string of terrible molecular events" that cause a person to develop lung cancer, says ScienceNews' Nathan Seppa. The protein — a variant of the Rac1 protein that is involved in cell proliferation — is activated by various other compounds and causes the cells in the lungs to behave in a malignant manner. The researchers say it could make for a good biomarker for lung cancer or for an early-treatment target because it shows up fairly early in the disease's development, Seppa says. "While the gene that encodes Rac1 routinely turns itself off after producing its protein, the variant gene making Rac1b doesn't," he adds.
The researchers examined lung tissue from smokers with lung cancer and found significantly higher levels of the protein in cancer cells as compared to close-by normal cells. "Tests in mice revealed that Rac1b gets activated by an enzyme called MMP3, which is involved in the breakdown and rebuilding of tissues such as collagen and elastin," Seppa says. "The mouse experiments indicated that MMP3 activation of Rac1b triggers another process by which lung-lining cells called epithelial cells abandon their posts and change behavior," a process that normally helps wounds to heal. What's still unclear, however, is the mechanism by which MMPs activate Rac1b. It's possible that smoke in the lungs draws the same kind of biological attention that a wound might, Seppa says, leading the body to want to "heal" the smoke as it would a wound.