前列腺癌
焦点粘着
癌症
转移
癌症研究
原癌基因酪氨酸蛋白激酶Src
萧条(经济学)
前列腺
生物
信号转导
基因敲除
肿瘤科
激酶
内分泌学
医学
内科学
细胞生物学
细胞凋亡
宏观经济学
经济
生物化学
作者
Yan Cheng,Xinghua Gao,Xian-Jing Li,Qiuhua Cao,Dandan Zhao,Jin‐Rong Zhou,Hongxi Wu,Yun Wang,Linjun You,Hongbao Yang,Yunlong He,Yongren Li,Jin‐Song Bian,Qingyi Zhu,Lutz Birnbaumer,Yong Yang
出处
期刊:Oncogene
[Springer Nature]
日期:2018-03-08
卷期号:37 (22): 2953-2966
被引量:55
标识
DOI:10.1038/s41388-018-0177-4
摘要
Depression drives cancer progression and induces poor clinical outcome. However, the mechanisms underlying depression and cancer outcomes are unclear. In this work, we investigated 98 prostate cancer patients and found that patients with high score of psychological depression were correlated with tumor invasion and metastasis. We found focal adhesion kinase (FAK) was increased in cancer patients with metastatic features and high score of depression. FAK knockdown completely blocked depression-promoted tumor invasion in orthotopic transplantation tumors. In Hi-myc mice and a murine model of depression, sympathetic activation was detected in the prostate tissue. Further we showed that FAK activation was dependent on a cAMP-PKA signaling pathway. Our results demonstrated that the activation of a sympathetic-FAK signaling pathway in prostate cancer patients with high degrees of depression facilitates tumor invasion. We suggest that blocking β2AR with propranolol or inhibiting FAK activation with PF562 271 may be novel strategies for depressed patients with invasive prostate cancer.
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