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Researchers at Fred Hutch Cancer Center have identified a previously overlooked molecular regulator that helps determine whether prostate tumors remain sensitive to treatment or evolve into a more aggressive, drug-resistant form of the disease.

The findings, published in Nature, reveal for the first time that a single transfer RNA, or tRNA, can control the identity of prostate cancer cells and influence their response to therapy.

"The discovery opens an entirely new realm of cancer biology that was previously unrecognized," said co-corresponding author Andrew Hsieh, a professor and associate director of Fred Hutch's Human Biology Division. "Historically, tRNAs have been thought to play a bystander role in cell maintenance and disease, but our study shows that tRNAs can actively shape the identity of cancer cells."

Prostate cancer, a leading cause of cancer in men, can shift cellular characteristics over time. Initially, prostate cancer depends on the activity of the androgen receptor, a protein that fuels tumor growth and is the primary target of standard therapies. But then many tumors shift to an androgen receptor–independent state. Once independent of the androgen receptor, prostate cancer tumors become more aggressive and less responsive to therapy.

Yeon Soo Kim, first author of the Nature paper and a Fred Hutch postdoctoral researcher in Hsieh's lab, sought to understand the molecular players underlying how prostate cancer changes its identity and becomes resistant to treatment.

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