Socialization slows cancer growth via a specific corticoamygdaloid pathway

Scientists from the Chinese Academy of Medical Sciences and the University of Minnesota have published a new report in Neuron showing that social interaction in mice slows the progression of breast cancer through a specific neural circuit between the prefrontal cortex and the basolateral nucleus of the amygdala (corticoamygdala circuit).

Experimental design and key findings

• Model: Immunocompetent mice with transplanted breast cancer cells.
• Conditions: “social” mice were kept in groups of 4–5 animals, and “loners” were kept one per cage.
• Result: with the same volume of initial transplantation, tumors in “loners” grew 60% faster than in socialized animals.

Neural basis of the effect

• Activation identification: Social interaction induced increased c-Fos in glutamatergic neurons of the anterior cingulate cortex (ACCGlu).
• Monotonic tracing: ACCGlu neurons project to the basolateral amygdala (BLAGlu).
• Chemogenetic modulation:
  • Inhibition of ACCGlu→BLAGlu using a DREADD inactivator significantly eliminated both the anxylolytic (anxiety-reducing) and antitumor effects of the social environment.
  • Selective activation of this circuit in isolated mice reproduced the benefits of socialization—reduced tumor growth and stress levels.

Mechanisms of action on the tumor

Researchers have noted that socialization:

1. Reduces stress levels (less cortisol), which has a beneficial effect on immune surveillance.
2. Enhances the cytotoxicity of NK cells and CD8⁺ T lymphocytes in the tumor microenvironment.
3. Stabilizes the barrier function of blood vessels inside the tumor, reducing metastasis.

Authors' statements

"Social connections activate a special corticoamygdala circuit in the brain that not only calms but also mobilizes anti-tumor immunity," says lead author Hui-Zhong Wen.

"Blocking this pathway completely abolishes the antitumor effect of socialization, highlighting its crucial role," adds co-author Xi-Yi Xiong.

The authors emphasize the following points:

• Cognitive-emotional integration
  “Our data demonstrate that the prefrontal cortex does not simply regulate emotions, but directly influences immunity,” notes Prof. Hui-Zhong Wen. “Social interaction activates ACC→BLA neurons, which begin to mobilize NK cells and CD8⁺ T lymphocytes against the tumor.”

• The Key Role of the ACCGlu→BLAGlu Chain
  “Chemogenetic inhibition of this pathway completely abolished the antitumor effect of socialization, highlighting its critical function,” adds Dr. Xi-Yi Xiong.

• Translatability of the result
  “We see great potential in developing neurostimulatory or pharmacological mimetics of social contact to support immunity in cancer,” says co-author Prof. Liu Jian.

• Clinical Significance
  “The results highlight that group psychosocial support programs may not only be emotionally beneficial but also biologically active elements of cancer therapy,” concludes Dr. Anna Chen.

Prospects

• Psychoneuroimmunology of oncology: these findings open the possibility of developing neurostimulation techniques or pharmaceutical mimetics of social interaction in the treatment of cancer.
• Clinical rehabilitation: Integrating group therapy and social support into postoperative and chemotherapy care protocols may improve prognosis.
• Targeted neuromodulation: It is promising to study transcranial magnetic or electrical stimulation of the ACC-BLAm circuit to enhance antitumor processes in the body.

This study highlights that the “social factor” is a real biological modifier of tumor growth and suggests a specific neural mechanism through which friendship and support can become part of complex oncotherapy.