AI Insight
Researchers identified a multi-step neural circuit connecting the brain's hypothalamus to prostate tumors through the vagus nerve and pelvic ganglion in mice. They found that different brain regions have opposing effects on tumor growth, with the paraventricular nucleus restraining tumors while the dorsal motor nucleus of the vagus promotes them through nerve cells in the major pelvic ganglion. These ganglion neurons release WNT3A protein, which stimulates cancer cell proliferation, and blocking this protein suppressed tumor-promoting effects.
Why it matters
This discovery reveals a previously unknown mechanism by which the brain can influence cancer progression through the nervous system. The findings suggest new therapeutic targets, including the neural circuit itself and the WNT3A pathway, which could potentially be manipulated to slow prostate cancer growth.
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⚠️ Preprint – Noch nicht peer-reviewed
Dieser Artikel wurde noch nicht von unabhängigen Experten begutachtet. Die Ergebnisse sind vorläufig und sollten mit Vorsicht interpretiert werden.
Brain-tumor communication is increasingly recognized. Peripheral autonomic nerves regulate prostate cancer progression, yet how the brain influences local nerve-tumor interactions remains unclear. We identify a polysynaptic circuit linking the hypothalamic paraventricular nucleus (PVN), dorsal motor nucleus of the vagus (DMV), major pelvic ganglion (MPG) and prostate tumor in mice. Although both nuclei were activated during tumor growth, PVN activity restrained, whereas DMV activity promoted tumor growth. MPG ablation abolished DMV-induced tumor promotion. Combining LMD with Smart-seq2 revealed transcriptional remodeling and increased Wnt3a expression in tumor-innervating, activated MPG neurons under upstream neural control. MPG explants released WNT3A, whose neutralization suppressed explant-induced cancer-cell proliferation. Together, our findings identify a polysynaptic PVN-DMV-MPG circuit that regulates prostate tumor growth and implicate WNT3A as a mediator of the pro-tumor effects of the MPG, highlighting the therapeutic potential of targeting the neural circuit and downstream molecular pathway.
Source: A polysynaptic hypothalamuspelvic-ganglion circuit regulates prostate tumor growth via WNT3A