Abstract:
:Molecular insights into how chronic stress affects lung tumorigenesis may offer new routes to chemoprevention. In this study, we show that chronic stress in mice chemically or genetically initiated for lung cancer leads to the release of norepinephrine and other catecholamines, thereby promoting lung tumorigenesis. Mechanistically, norepinephrine induced phosphorylation of L-type voltage-dependent calcium channels (VDCC) through the β-adrenergic receptor-PKA pathway. VDCC triggered calcium mobilization, thereby inducing activation of IGF-1R via exocytosis of insulin-like growth factor 2 (IGF2). Mice expressing lung-specific IGF-1R exhibited accelerated lung tumor development in response to chronic stress. Notably, clinically approved antihypertensive drugs that block L-type VDCC prevented the effects of chronic stress or norepinephrine on the IGF2/IGF-1R signaling cascade, along with transformation of lung epithelial cells and lung tumor formation. Overall, our results identify an actionable mechanism to limit the effects of chronic stress on lung tumorigenesis. Cancer Res; 76(22); 6607-19. ©2016 AACR.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Jang HJ,Boo HJ,Lee HJ,Min HY,Lee HYdoi
10.1158/0008-5472.CAN-16-0990subject
Has Abstractpub_date
2016-11-15 00:00:00pages
6607-6619issue
22eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-16-0990journal_volume
76pub_type
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