Scientists at Sanford-Burnham Medical Research Institute have identified how an enzyme called PKCζ suppresses prostate tumor formation. The finding, which also describes a molecular chain of events that controls cell growth and metastasis, could lead to novel ways to control disease progression.
Working together, the labs of Maria T. Diaz-Meco, PhD, and Jorge Moscat, PhD, found that PKCζ controls the activation of a pro-tumor gene called c-Myc. Normally, PKCζ's alteration keeps c-Myc in check. But PKCζ levels are low in prostate and other cancers, leaving c-Myc free to enhance cell growth and metastasis. This study, published in the Proceedings of the National Academy of Sciences, suggests that restoring PKCζ could provide a new approach to treating prostate cancer.
The researchers found that PKCζ suppresses tumors in cooperation with a gene called PTEN. PTEN has been long known to act as a tumor suppressor, and it's also well-established that its mutated form is common in prostate cancer. But the loss of normal PTEN function alone doesn't lead to aggressive prostate cancer. According to this study, the loss of PKCζ and the resulting overactive c-Myc are also needed for aggressive prostate cancer to develop.
Potential approaches toward attacking prostate cancer may in the future involve activating PKCζ through gene therapy, or dealing with its inaction downstream—perhaps by finding another way to inhibit c-Myc in the absence of PKCζ. Read the study abstract.
