Neuron-Tumour Communication Fuels Aggressive Cancer Growth, New Studies reveal
BOSTON, MA – In a surprising twist, research published in Cancer Cell (2017) and Nature (2025) demonstrates that signals exchanged between neurons and tumour cells are actively driving the growth of small cell lung cancer (SCLC), a notably aggressive and treatment-resistant form of the disease, and its spread to the brain. the findings challenge conventional understanding of cancer progression and open new avenues for therapeutic intervention.
SCLC, responsible for roughly 25-30% of all lung cancer cases, is notorious for its rapid growth and early metastasis, frequently spreading to the brain. Despite initial responses to chemotherapy, recurrence is almost universal, with a median survival rate of just over a year post-diagnosis. Now, scientists have uncovered a critical mechanism: cancerous cells aren’t acting alone. They’re receiving and responding to cues from the nervous system, effectively hijacking neuronal signalling pathways to accelerate their proliferation and metastatic potential. This discovery suggests that targeting thes neuron-tumour interactions could considerably improve outcomes for patients battling this devastating disease.
Researchers, led by Gabriella mollaoglu at the University of Helsinki, frist identified that SCLC cells express receptors for neurotransmitters – chemical messengers used by neurons. Specifically, they found that SCLC cells respond to acetylcholine, a neurotransmitter involved in nerve impulse transmission. This interaction triggers a cascade of events within the cancer cells, promoting their growth and survival. The 2017 Cancer Cell study detailed how blocking acetylcholine signalling in preclinical models significantly reduced tumour growth and prolonged survival.
Further investigation, published in Nature in 2025 by A.S. Ireland and colleagues, revealed a more complex interplay. The team demonstrated that SCLC cells not only receive signals from neurons but also influence neuronal activity, creating a feedback loop that amplifies tumour progression. This bidirectional communication is particularly pronounced in the brain, where SCLC frequently metastasizes, establishing a microenvironment that actively supports cancer cell survival and expansion.
“We’ve shown that the nervous system isn’t just a bystander in cancer progression; it’s an active participant,” explains Ireland. “This opens up exciting possibilities for developing therapies that disrupt these neuron-tumour circuits, perhaps slowing down or even preventing the spread of this deadly cancer.”
The research teams are now focused on identifying specific targets within these signalling pathways and developing novel therapeutic strategies, including drugs that block neurotransmitter receptors or disrupt neuronal activity in the tumour microenvironment. Clinical trials are anticipated to begin within the next few years, offering a glimmer of hope for patients with limited treatment options.
