肺癌合并抑郁症的患者在精神压力下导致肿瘤侵袭和转移、加速患者死亡。其确切机制尚未阐明。研究证实, 抑郁刺激5-羟色胺分泌影响机体免疫功能、促进肿瘤生长。本课题组通过128名抑郁相关性肺癌患者及非抑郁肺癌患者分析，发现抑郁相关性肺癌患者5-HT水平增高；生存时间缩短与5HT1R呈负相关。P62下调、BECN1上调、STAT3活化上调B7-H1, B7-H2等抑制性信号导致肿瘤特异性T细胞活性降低。据此推测“5-HT/5HT1aR是抑郁相关性肺癌诱导免疫逃逸的关键因素， p62-STAT3自噬信号是抑郁相关性肺癌抵抗特异性T细胞杀伤的重要通路”。本课题拟利用患者样本、5HT1aR敲除细胞结合抑郁荷瘤模型, 从整体、细胞及分子水平上探讨5-HT/5-HT1aR与抑郁相关性肺癌诱导免疫抑制及激活p62-STAT3自噬抵抗特异性T细胞杀伤的分子机制，为抑郁相关性肺癌患者治疗提供一种新思路。

During chronic stress the lung cancer patients with depression like behaviors can cause tumor invasion and metastasis, and the final and fatal step in the progression, but the underlying mechanisms remain poorly understood. Depression, a chronic stress factor, can stimulate the secretion of 5-HT, can affect the immune function and promote the growth of tumor. Here 64 human lung cancer patients with major depression and 64 human lung cancer patients individuals were recruited in the study, tumor the level of 5-HT was increased, and the survival time was significantly correlated with the expression of 5-HT1aR. Downregulation of P62, up regulation of BECN1, activation of STAT3 induce B7-H1, B7-H2 and other inhibitory signals resulted in the decrease of specific T cell lysis. However, supposedly“5-HT/5HT1aR is a key factor to induce tumor immune escape, and p62-STAT3 autophagy signaling is an important pathway for the specific T cell killing in the lung cancer patients with depression”. The study intends to using clinical samples, cells of knockdown 5HT1aR with depression for tumor model, from the organization, cell and molecular level to study the molecular mechanisms between 5-HT/5-HT1aR induce tumor immune escape and autophagy induced activation of p62-STAT3 resistance specific T cell killing for the lung cancer patients with depression like behaviors, which provides a new way for the lung cancer patients with depression.