In the research community, MYC is historically known to be a difficult oncogene to target in cancer therapy. However, a recent study in the Journal of Cell Biology has found that an enzyme called PHLPP2 can serve as a potential route to target the MYC gene.
Histology slide of prostate cancer showing both benign glands and prostate carcinoma. Credit: Oncolex.org
"Now, we have a new way of getting at this old foe in cancer research," said Cold Spring Harbor Laboratory (CSHL) researcher Lloyd Trotman, who was focused on a cure for prostate cancer--one of the most prevalent cancers among men and the second leading cause of cancer death in American men.
Prostate cancer can metastasize to other parts of the body and patients with metastatic cancer have a much-reduced rate of survival than if the cancer was contained in the organ.
Now the study, co-led by Dr. Trotman and Dr. Dawid Nowak, an assistant professor at Weill Cornell and a former postdoctoral fellow at the Trotman lab, was able to examine the natural process of prostate cancer metastasis in mice and how to halt these processes by deleting the PHLPP2 enzyme.
The PHLPP2 enzyme is a critical protein in a signal pathway implicated in cell growth and survival in response to extracellular communications and signal relays. For prostate cancer, PHLPP2 cause the progression and later metastasis because it stabilizes and supports the MYC oncogene. Thus, blocking PHLPP2 can be proven as a viable drug target for the treatment of prostate cancer as it can halt the progression of cancer growth and metastasis. In addition, deleting the enzyme didn't show any symptoms of toxicity in mice or human cells.
Source: Cold Spring Harbor Laboratory