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The monoamine oxidase A (MAOA) enzyme, a target for antidepressants, shows indications that it may also promote prostate cancer growth.

  
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An animal study, published in the July 1 issue of Journal of Clinical Investigation (2014;124:2891-1908), found that suppressing MAOA could reduce or even eliminate prostate tumor growth and metastasis.

 

"When this enzyme is not suppressed, it produces a tumor-rich environment that fuels the growth and metastasis of prostate cancer cells," Leland Chung, PhD, corresponding author of the paper and Director of the Uro-Oncology Research Program at Cedars-Sinai Samuel Oschin Comprehensive Cancer Institute, explained in a news release. "Suppressing this enzyme and combining it with current therapies may provide a better way to manage and cure men with metastatic prostate cancer."

 

MAOA regulates the amount of neurotransmitters in the central nervous system by deactivating and breaking them down, he continued. "Like all enzymes in the brain, MAOA is needed in optimum quantities to work effectively on patients. Previous studies have shown that too much MAOA is linked with depression, while too little is linked with autism, aggression and anxiety.

 

The study's first author is Jason Boyang Wu, PhD, a postdoctoral fellow. "Our study demonstrates for the first time to our knowledge that MAOA induces EMT [epithelial-to-mesenchymal transition] and augments hypoxic responses to increase the migratory, invasive, and metastatic potential of prostate cancer cells," he and his colleagues wrote.

 

"The molecular basis of MAOA action could serve as a prognostic biomarker for poor differentiation and increased aggressiveness in prostate cancer. Targeting MAOA and disengaging its downstream signaling network driving EMT, hypoxia, and oxidative stress provides a promising mechanistic rationale for therapeutic development."

 

The research was funded by the National Institutes of Health, the Department of Defense, the USC-Taiwan Center for Translational Research, and the Daniel Tsai Family Fund.