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A multi-institutional collaborative study led by researchers at the University of Chicago and the Fred Hutchinson Cancer Center has identified a previously unknown biological mechanism that controls cell identity and treatment resistance in advanced prostate cancer.

Published in Nature, the study reveals that a specific transfer RNA (tRNA) named tRNAArg (UCU)-1 plays a central role in allowing prostate cancer cells to escape targeted therapies and transition into more aggressive and treatment-resistant forms of the disease. This finding could help researchers develop a way to resensitize resistant tumors to existing therapies.

Prostate cancer, the second-leading cause of cancer death among men in the United States, often depends on androgen receptor signaling for tumor growth. Many tumors initially respond to androgen deprivation therapies and androgen receptor pathway inhibitors like enzalutamide, apalutamide and darolutamide. Over time, some tumors adapt through a process known as lineage plasticity, where cancer cells lose their dependence on androgen signaling and acquire features of neuroendocrine prostate cancer, a form of cancer that is resistant to therapy.

The molecular cues that drive this kind of transformation have remained poorly understood. Using high-resolution RNA sequencing, the research team at the University of Chicago analyzed samples from patients, animal models and prostate cancer cells and found that tRNAArg (UCU)-1, a small noncoding RNA molecule that helps cells make proteins, is consistently depleted as tumors transition from a therapy-responsive to a therapy-resistant state.

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