A team of researchers at Roswell Park Comprehensive Cancer Center has identified a potential new treatment target for neuroendocrine prostate cancer (NEPC), a rare and aggressive subtype resistant to traditional therapies. The study, published in Oncogene, focuses on the role of HSP60, a protein involved in maintaining mitochondrial function.

NEPC develops when prostate cancer cells evolve in response to androgen deprivation therapy (ADT), transforming into a form that no longer relies on androgen signaling. These neuroendocrine cells are inherently resistant to standard treatments like cisplatin and other chemotherapies.

By inhibiting HSP60, researchers found that β-catenin signaling—a pathway known to drive cancer stemness and metastasis—was significantly reduced. This disruption caused neuroendocrine cells to revert to a cisplatin-sensitive state and decreased tumor burden in preclinical models. Additionally, HSP60 inhibition improved sensitivity to other mitochondrial-toxic drugs like doxorubicin.

Importantly, targeting HSP60 could leverage existing drugs, offering a more immediate path to clinical application.

This research offers a promising step toward personalized treatments for patients with advanced prostate cancer, providing hope where current therapies fall short.

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