Prostate cancer hijacks the normal prostate's growth regulation program to release the brakes and grow freely, according to Weill Cornell Medicine researchers. The discovery, published Dec. 13 in Nature Communications, paves the way for new diagnostic tests to guide treatment and could also help drug developers identify novel ways to stop the disease.
A protein called the androgen receptor normally functions to guide the development of the prostate—signaling the cells to stop growing, act as normal prostate cells and maintain a healthy state. The receptor is activated by androgens or sex hormones like testosterone, which triggers the receptor to bind to DNA, causing the expression of some genes and suppression of others. But in cancer, the androgen receptor is reprogrammed to tell the cells to continue growing, driving tumor development.
It's pretty well known in the field that the androgen receptor gets hijacked in a variety of ways and starts taking on new functions to drive prostate cancer cell growth." Dr. Christopher Barbieri, senior author, the Peter M.
Sacerdote Distinguished Associate Professor in Urologic Oncology, associate professor of urology and member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine This study showed that androgen receptors in prostate cells can work as either an accelerator speeding cell growth or a brake inhibiting it. Tumors redirect the receptors' normal activity to press the accelerator and release the brake. Uncover.
