In a recent study from Washington State University, researchers find a way that prostate cancer cells hijack the body’s bone maintenance.
This could trigger the spread of bone cancers present in 90% of prostate-cancer fatalities.
In the study, the research team introduced human prostate cancer cell lines in mice.
They saw a particular enzyme called MAOA activate a cascade of signals that made it easier for tumor cells to invade and grow in bone.
Ordinarily, bone is built up by cells called osteoblasts and reabsorbed during growth and healing by cells called osteoclasts.
But the MAOA enzyme triggers three proteins that enhance the function of the destructive osteoclasts.
This means the cancer cells can specifically activate the osteoclasts for bone degradation.
When they reduced this enzyme expression in prostate cancer cells, they found a lower prostate cancer bone metastasis.
On the other hand, when they increased this enzyme in prostate cancer cells, they found increased bone metastasis.
The researchers used a drug called clorgyline to inhibit the activity of the MAOA enzyme; the drug disrupted the signaling system that led to cancer cell invasion and proliferation.
Interestingly, the researchers found that the process appears to respond to the same drugs found in certain antidepressants.
The study provides a rationale to pursue the new use of ‘old’ antidepressant drugs to help late-stage prostate cancer patients with cancer metastasis.
The team suggests that their findings provide promising results, and that their future work will adjust the formulation, dose and delivery route of MAOA inhibitors.
They hope the findings could help develop new treatment for prostate cancer metastasis.
Jason Wu, an assistant professor of pharmacy at WSU Spokane, is a study author.
The findings are published in the journal Cancer Cell.
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