TRβ receptor could be key to slowing prostate cancer

Prostate cancer is the second most common cancer among men worldwide. Early-stage disease is often treated by lowering testosterone levels, but many patients eventually become resistant to this approach. For these individuals, treatment options are limited, highlighting the importance of research into alternative therapies.

A new study has discovered a hormone produced by the thyroid gland which may play a key role in the development of prostate cancer. The international research conducted by Umeå University and the Medical University of Vienna suggests that blocking a specific receptor for this hormone can inhibit the growth of tumour cells in the prostate, potentially leading to new ways of treating aggressive forms of the disease.

“The results indicate that the receptor in question is a driving force in the growth of cancer. Substances that block it could thus be a target for future drugs against prostate cancer,” said Lukas Kenner, visiting professor at Umeå University and the lead researcher of the study.

The role of thyroid hormone receptor beta

The receptor identified by the research team is thyroid hormone receptor Beta, or TRβ, which binds to the thyroid hormone triiodothyronine, known as T3. Laboratory experiments demonstrated that activation of T3 caused a sharp increase in the number of prostate cancer cells.

However, when TRβ was inhibited using a research compound called NH-3, the growth of cancer cells was significantly reduced. NH-3 is currently used only in research to block TRβ, but the findings suggest it could have therapeutic potential in the future.

Promising results in animal studies

The study’s findings were further validated through experiments in mice. Tumours treated with NH-3 either remained smaller or progressed more slowly, particularly in models of castration-resistant prostate cancer. This aggressive form of the disease continues to grow despite treatments that lower testosterone, making it especially difficult to treat clinically.

Blocking TRβ with NH-3 was shown to work by eliminating a key signal known as the androgen receptor signal. This signal is normally activated by testosterone and plays a central role in the development of prostate cancer.

Supporting evidence from patient data

The research team also analysed tissue samples from prostate cancer patients. Elevated levels of TRβ were observed in tumour tissue compared with healthy prostate tissue. Genetic studies further revealed that mutations in many patients alter thyroid hormone signalling pathways, indicating that targeting the thyroid hormone and its receptor could be an encouraging target for new treatments.

“Of course, it is a balancing act not to change the hormonal balance in the thyroid gland more than necessary to fight cancer in another part of the body, and it will probably not be a solution for all types of prostate cancer. Further research will have to answer what a treatment could look like, possibly in combination with other treatments. Of course, this is an interesting track,” said Kenner.

The urgent need for new treatments

Identifying TRβ’s role in prostate cancer growth represents a major moment in understanding the disease. The findings could help scientists develop new and more effective treatments for patients with aggressive or treatment-resistant cancers.