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Social interaction in mice suppresses breast cancer progression via a corticoamygdala neural circuit
Hui-Zhong Wen1, Si-Yi Xiong2, Yun-Xiao Lou1
1Department of Neurobiology, Chongqing Key Laboratory of Brain Development and Cognitive Science, Army Medical University, Chongqing 400038, China.
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.
Insights
Social interaction (SI) suppresses tumor growth by activating a brain circuit from the anterior cingulate cortex to the basolateral amygdala. This pathway inhibits sympathetic nerve activity, offering new insights for cancer treatment.
Area of Science:
- Neuroscience
- Immunology
- Oncology
Background:
- Social interaction (SI) is crucial for mammals and linked to improved cancer outcomes.
- The neural mechanisms underlying the anti-cancer effects of SI are not well understood.
Purpose of the Study:
- To elucidate the neural circuits through which social interaction influences tumor progression.
- To investigate the role of the anterior cingulate cortex (ACC) and basolateral amygdala (BLA) in mediating these effects.
Main Methods:
- Utilized mouse models to study the effects of SI on tumor growth.
- Employed chemogenetics to manipulate specific neural circuits (ACC glutamatergic neurons projecting to BLA).
- Measured changes in sympathetic nerve activity, norepinephrine levels, and antitumor immunity.
Main Results:
- SI suppressed tumor growth by activating ACC glutamatergic neurons projecting to the BLA.
- Inhibition of this ACC→BLA circuit abolished the anxiolytic and antitumor effects of SI.
- Artificial reactivation of the ACC→BLA circuit mimicked the beneficial effects of SI.
- Modulation of this circuit affected tumor progression via sympathetic activity and norepinephrine release, impacting antitumor immunity.
Conclusions:
- Social interaction activates a cortico-amygdala neural circuit (ACC→BLA) that inhibits tumor progression.
- This circuit functions by reducing intratumoral sympathetic activity and modulating antitumor immunity.
- Findings suggest potential therapeutic applications of social support in cancer treatment by targeting this neural pathway.
