Newly identified tumor suppressor provides therapeutic target for prostate cancer

Apr. 1, 2013 ? Researchers have identified how an enzyme called PKC? (PKCzeta) 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 in close collaboration, the labs of Maria T. Diaz-Meco, Ph.D., and Jorge Moscat, Ph.D., found that PKC? controls the activation of a pro-tumor gene called c-Myc. Normally, PKC?'s alteration keeps c-Myc in check. But PKC? levels are low in prostate and other cancers, leaving c-Myc free to enhance cell growth and metastasis. This study, appearing online April 2 in the Proceedings of the National Academy of Sciences, suggests that restoring PKC? could provide a new approach to treating prostate cancer.

How PKC? acts as a prostate tumor suppressor

Previous studies suggested that PKC? might act as a tumor suppressor -- but that wasn't clear in the case of prostate cancer. In their study, the team learned of PKC?'s role after genetically engineering mice so they lacked the enzyme altogether.

"In this study, we assessed the role of PKC? in prostate cancer, and for the first time we used a knockout mouse for PKC? to demonstrate that it's actually a tumor suppressor," Diaz-Meco said. "But, I think the major advance in this paper is that we found out how PKC? is a tumor suppressor in prostate cancer."

In their study, the researchers found that PKC? 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 PKC? and the resulting over-active c-Myc are also needed for aggressive prostate cancer to develop.

Potential approaches toward attacking prostate cancer may in the future involve activating PKC? through gene therapy, or dealing with its inaction downstream -- perhaps by finding another way to inhibit c-Myc in the absence of PKC?.

This research was funded by the U.S. National Institutes of Health (National Cancer Institute grants R01CA134530, R01CA132847, and 5P30CA030199-31; National Institute of Allergy and Infectious Diseases grant R01AI072581; National Institute of Diabetes and Digestive and Kidney Diseases grant R01DK088107) and the Department of Defense (grant DoD-PC080441).

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Story Source:

The above story is reprinted from materials provided by Sanford-Burnham Medical Research Institute. The original article was written by Bruce Lieberman.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

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Journal Reference:

1. Ji Young Kim, Tania Valencia, Shadi Abu-Baker, Juan Linares, Sang Jun Lee, Tomoko Yajima, Jing Chen, Alexey Eroshkin, Elias A. Castilla, Laurence M. Brill, Mario Medvedovic, Michael Leitges, Jorge Moscat, and Maria T. Diaz-Meco. c-Myc phosphorylation by PKC? represses prostate tumorigenesis. Proceedings of the National Academy of Sciences, 2013; DOI: 10.1073/pnas.1221799110

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/health_medicine/genes/~3/yQtUT01C0No/130401181504.htm

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