Lung cancer results in more patient deaths each year than any other cancer type. Additional treatment strategies are needed to improve clinical responses to approved treatment modalities and prevent the emergence of resistant disease. Catecholamines including norepinephrine and epinephrine are elevated as a result of chronic stress and mediate their physiological effects through activation of adrenergic receptors on target tissues. Lung cancer cells express β-adrenergic receptors (β-ARs), and numerous preclinical studies indicate that β2-AR signaling on lung cancer cells facilities cellular programs including proliferation, motility, apoptosis resistance, epithelial-to-mesenchymal transition, metastasis, and the acquisition of an angiogenic and immunosuppressive phenotype. Here, we review the preclinical and clinical evidence supporting a potential role for beta-blockers in improving the clinical outcome of lung cancer patients.

Catecholamines including norepinephrine and epinephrine act of β-ARs expressed on NSCLC tumor cells and activate pathways regulating tumor progression.

中文翻译：

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肺癌中的β-肾上腺素信号传导：β-受体阻滞剂的潜在作用。

肺癌每年导致的患者死亡人数超过任何其他癌症类型。需要其他治疗策略来改善对批准的治疗方式的临床反应并预防耐药性疾病的出现。由于慢性应激，儿茶酚胺（包括去甲肾上腺素和肾上腺素）升高，并通过激活靶组织上的肾上腺素能受体来介导其生理作用。肺癌细胞表达β-肾上腺素能受体（β-ARs），许多临床前研究表明，肺癌细胞上的β2-AR信号传导促进细胞程序的增殖，运动，凋亡抗性，上皮-间质转化，转移和获得血管生成和免疫抑制表型。这里，

儿茶酚胺（包括去甲肾上腺素和肾上腺素）作用于在NSCLC肿瘤细胞上表达的β-ARs，并激活调节肿瘤进展的途径。