Social interaction in mice suppresses breast cancer progression via a corticoamygdala neural circuit.

Neuron 2025

Wen HZ, Xiong SY, Lou YX, Yang SZ, Sun L, Yi YL, Tang BQ, Shu Q, Wang ZQ, Yan XJ, Wu YR, Chen PH, Qi XW, Zhang Y, Dai LM, Xiong Y, Wu GY

Abstract

Social behaviors are vital for all mammalian species. Clinical observations and epidemiological studies have demonstrated that social interaction (SI) may slow cancer progression and improve patient outcomes. However, the underlying neural mechanisms remain unknown. Here, we found that SI in mouse models suppresses tumor growth through activating glutamatergic inputs from the anterior cingulate cortex (ACCGlu) to the basolateral amygdala (BLA), inhibiting intratumoral sympathetic nerve activity. Chemogenetic inhibition of the SI-activated ACCGlu neurons and ACCGlu→BLAGlu circuits abolished anxiolytic and antitumor effects of SI. Artificial reactivation of these neurons and circuits could mimic the anxiolytic and antitumor effects of SI. Manipulating the ACCGlu→BLAGlu circuits to regulate intratumoral sympathetic activity and norepinephrine (NE) release affected tumor progression by modulating antitumor immunity. Collectively, our study shows that SI activates the corticoamygdala neural circuit, which suppresses cancer progression, offering potential insights into the clinical application of social support in cancer treatment.

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