Increasing evidence indicates that cancer-induced anxiety can promote tumor progression, but the underlying neural mechanisms are unclear. A new study shows that tumor-bearing mice exhibit anxiety-like behaviors and identifies a direct tumor–nerve crosstalk that controls anxiety-promoting tumor progression. The researchers used several mouse models of breast cancer and neuroscience approaches, including pharmacogenetic, optogenetic and chemogenetic approaches, to demonstrate the role of corticotropin-releasing hormone (CRH) neurons in the central medial amygdala (CeM) in cancer-induced anxiety and tumor progression. Notably, ablation or inhibition of CeM^CRH neurons and the CeM^CRH – lateral paragigantocellular nucleus (LPGi) circuit markedly decreased anxiety-like behaviors and tumor growth, while activation of the CeM^CRH – LPGi resulted in opposite effects. Alprazolam, an antianxiety drug, inhibited the activity of CeM^CRH neurons, reduced cancer-induced anxiety and slowed the progression of cancer in mammary tumor–bearing mice, opening a new potential avenue for the treatment of breast cancer.

越来越多的证据表明癌症引起的焦虑可以促进肿瘤进展，但潜在的神经机制尚不清楚。一项新的研究表明，荷瘤小鼠表现出类似焦虑的行为，并确定了一种直接的肿瘤神经串扰，可以控制焦虑促进的肿瘤进展。研究人员使用了几种乳腺癌小鼠模型和神经科学方法，包括药物遗传学、光遗传学和化学遗传学方法，以证明中央内侧杏仁核（CeM）中促肾上腺皮质激素释放激素（CRH）神经元在癌症引起的焦虑和肿瘤进展中的作用。值得注意的是，消融或抑制 CeM ^CRH神经元和 CeM ^CRH – 外侧副巨细胞核 (LPGi) 回路可显着减少焦虑样行为和肿瘤生长，而激活 CeM ^CRH – LPGi 会产生相反的效果。阿普唑仑是一种抗焦虑药物，可抑制 CeM ^CRH神经元的活性，减少癌症引起的焦虑，并减缓患有乳腺肿瘤的小鼠的癌症进展，为乳腺癌的治疗开辟了新的潜在途径。