Interrelations between psychological stress and cancer - deciphering molecular signals in the tumor microenvironment

Current research has revealed some links between psychological stress and cellular mutation, neoplastic proliferation and metastasis in patients with cancer. In stressful situations, the stress-related neuroendocrine mediators (e.g., catecholamines, and glucocorticoids (GSs)) are being secreted, via stimulation of the sympathetic nervous system (SNS), and the hypothalamic-pituitary-adrenocortical (HPA) axis. Catecholamine may affect the malignant progression, since they can regulate various cellular signaling pathways, via adrenergic receptors (ARs) that are expressed by different types of neoplastic cells. The ARs increase the proliferation and invasive potential of such cells, and  change their “behavior” in the tumor microenvironment. Similarly, cortisol and its glucocorticoid receptors (GRs) can promote stress-induced malignant growth and metastasis. Maladaptation to stressful situations, often relevant to the cancer diagnosis and treatment, may accelerate tumor growth and spread (e.g., via inflammation, angiogenesis, and migration). Studies have shown that psychological interventions can be helpful for adaptation to adverse circumstances during the therapeutic process in patients with cancer. This mini-review will address some interrelations between psychological stress and cancer. It will discuss how the receptor-mediated signaling pathways may lead to cancer initiation, propagation, and spread. In addition, it will describe a supportive role of the stress reduction strategies (e.g., in patients with breast cancer (BC).