We are a nation of anxious people. Ten percent of Americans take antidepressants, and more than 60 percent of those people have taken them for 2 years or longer.
Usually stats like these are a cause for hand-wringing, but new information about how antidepressants may work against prostate cancer may be putting a new spin on everything.
Scientists have discovered an enzyme that assists prostate cancer in spreading into bones. They have also learned that many antidepressants contain agents that block the production of that enzyme.
It is usually the bones which see the first spread of metastasizing prostate cancer. Accordingly, approximately 90 percent of all prostate cancer deaths involve bone metastasis.
The new study describes how the enzyme MAOA triggers a signaling cascade that simplifies the process by which prostate cancer cells spread to the bone. It stimulates three proteins to amplify the function of osteoclasts. These are bone cells that play a role in the degradation of bone tissue during growth and healing.
Lower the incidence of MAOA, the researchers found, and you reduce the cells' ability to spread to the bone. Conversely, increasing the incidence of MAO in prostate cancer cells, and increased bone metastasis was found in mice.
When the scientists introduced a drug known as clorgyline – an antidepressant known to block MAOA – into the prostate cancer lines, they noted how the drug prevented MAOA from activating the three proteins that enhance osteoclast function.
Accordingly, the ability of prostate cells' ability to metastasize and grow into the skeletal structure was diminished.
Clorgyline is not the only antidepressant in clinical use that works the way it does. Among the research team's next steps is working through that list of drugs and seeing what effect they have on cancer metastasis.
Further investigation and adjustments in testing such as formulation, dosage, and delivery route of MAOA inhibitors is ongoing.
If you’d like to learn more prostate cancer research, please visit our website today!
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