Public release date: 12-Apr-2010
Chronic stress has recently been implicated as a factor that may accelerate the growth of tumors. However, the mechanisms underlying this effect have not been determined. But now, Anil Sood and colleagues, at the University of Texas MD Anderson Cancer Center, Houston, have generated data using human ovarian cancer cell lines and tumor specimens that indicate that stress hormones, especially norepinephrine and epinephrine, can contribute to tumor progression in patients with ovarian cancer. They therefore suggest that targeting stress hormones and the signaling pathways that they activate might be of benefit to individuals with cancer.
Anoikis is the process by which cells are triggered to die when separated from their surrounding matrix and neighboring cells. Tumor cells that spread to other sites somehow escape anoikis. In the study, exposure of human ovarian cancer cells lines to either of the stress hormones norepinephrine or epinephrine protected them from anoikis. Similarly, in a mouse model of ovarian cancer, restraint stress and the associated increases in norepinephrine and epinephrine protected the tumor cells from anoikis and promoted their growth. This effect was associated with activation of the protein FAK. The clinical significance of these data was highlighted by the observation that in human ovarian cancer patients, behavioral states related to greater stress hormone activity were associated with higher levels of activated FAK, which was in turn linked to substantially accelerated mortality.