Journal
CURRENT PHARMACEUTICAL DESIGN
Volume 22, Issue 16, Pages 2389-2402Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1381612822666160226144025
Keywords
Psychological stress; cancer; tumor microenvironment; adrenergic receptor; catecholamine; anticancer drug
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Funding
- Brain Korea 21 Plus - Ministry of Education, Korea [2.140011.01]
- National Research Foundation of Korea (NRF) - Korean government [2010-0028684]
- National Research Foundation of Korea [2010-0028684, 22A20130012280, 21A20131212415] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Psychological stress is an emotion experienced when people are under mental pressure or encounter unexpected problems. Extreme or repetitive stress increases the risk of developing human disease, including cardiovascular disease (CVD), immune diseases, mental disorders, and cancer. Several studies have shown an association between psychological stress and cancer growth and metastasis in animal models and case studies of cancer patients. Stress induces the secretion of stress-related mediators, such as catecholamine, cortisol, and oxytocin, via the activation of the hypothalamic-pituitary-adrenocortical (HPA) axis or the sympathetic nervous system (SNS). These stress-related hormones and neurotransmitters adversely affect stress-induced tumor progression and cancer therapy. Catecholamine is the primary factor that influences tumor progression. It can regulate diverse cellular signaling pathways through adrenergic receptors (ADRs), which are expressed by several types of cancer cells. Activated ADRs enhance the proliferation and invasion abilities of cancer cells, alter cell activity in the tumor microenvironment, and regulate the interaction between cancer and its microenvironment to promote tumor progression. Additionally, other stress mediators, such as glucocorticoids and oxytocin, and their cognate receptors are involved in stress-induced cancer growth and metastasis. Here, we will review how each receptor-mediated signal cascade contributes to tumor initiation and progression and discuss how we can use these molecular mechanisms for cancer therapy.
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