HomeHealth & FitnessNew hope as prostate cancer’s hidden enzymes may hold key to beating drug resistance

New hope as prostate cancer’s hidden enzymes may hold key to beating drug resistance

Scientists have uncovered a critical weakness in prostate cancer’s defences. The disease relies on two enzymes, PDIA1 and PDIA5, to survive and resist treatment. When these enzymes are blocked, cancer cells lose their strength and die, making existing drugs far more powerful. Here’s how it helps in fighting drug-resistant prostate cancer:

November 11, 2025 / 13:01 IST
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Cure for prostate cancer: Scientists caution that the current enzyme-blocking drugs need refining before they can be used safely in people. Some versions still affect healthy cells (Image: Pexels)
Cure for prostate cancer: Scientists caution that the current enzyme-blocking drugs need refining before they can be used safely in people. Some versions still affect healthy cells (Image: Pexels)

When a dull ache in the lower back, and frequent trips to the loo become the new normal in men, the signs can point to prostate cancer. It is a disease that starts in the prostate gland but can spread and become life-threatening if not caught early.

In a recent discovery, scientists from Australia’s Flinders University and South China University of Technology have found a hidden weakness inside prostate cancer cells, one that could make them self-destruct. The team discovered that prostate cancer cells rely on two enzymes, PDIA1 and PDIA5, to keep themselves alive. These enzymes act like bodyguards for the androgen receptor (AR), a protein that fuels the growth of prostate tumours. When the enzymes were blocked, the AR began to fall apart — and with it, the cancer cells.

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In both lab experiments and mouse models, tumours shrank dramatically. Even better, when these enzyme blockers were used alongside an existing prostate cancer drug called enzalutamide, the results were even stronger. Professor Luke Selth from Flinders University said, “By targeting these enzymes, we can destabilise the AR and make tumours more vulnerable to existing therapies.”

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