Vignjević Petrinović Sanja, Milošević Maja S, Marković Dragana, Momčilović Sanja
Group for Neuroendocrinology, Institute for Medical Research, National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Group for Immunology, Institute for Medical Research, National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Front Physiol. 2023 Mar 20;14:1119095. doi: 10.3389/fphys.2023.1119095. eCollection 2023.
Stress is an integral part of life. While acute responses to stress are generally regarded as beneficial in dealing with immediate threats, chronic exposure to threatening stimuli exerts deleterious effects and can be either a contributing or an aggravating factor for many chronic diseases including cancer. Chronic psychological stress has been identified as a significant factor contributing to the development and progression of cancer, but the mechanisms that link chronic stress to cancer remain incompletely understood. Psychological stressors initiate multiple physiological responses that result in the activation of the hypothalamic-pituitary-adrenal (HPA) axis, sympathetic nervous system, and the subsequent changes in immune function. Chronic stress exposure disrupts the homeostatic communication between the neuroendocrine and immune systems, shifting immune signaling toward a proinflammatory state. Stress-induced chronic low-grade inflammation and a decline in immune surveillance are both implicated in cancer development and progression. Conversely, tumor-induced inflammatory cytokines, apart from driving a tumor-supportive inflammatory microenvironment, can also exert their biological actions distantly circulation and therefore adversely affect the stress response. In this minireview, we summarize the current findings on the relationship between stress and cancer, focusing on the role of inflammation in stress-induced neuroendocrine-immune crosstalk. We also discuss the underlying mechanisms and their potential for cancer treatment and prevention.
压力是生活中不可或缺的一部分。虽然对压力的急性反应通常被认为有助于应对即时威胁,但长期暴露于威胁性刺激会产生有害影响,并且可能是包括癌症在内的许多慢性疾病的一个促成因素或加重因素。慢性心理压力已被确定为导致癌症发生和发展的一个重要因素,但将慢性压力与癌症联系起来的机制仍未完全了解。心理压力源引发多种生理反应,导致下丘脑-垂体-肾上腺(HPA)轴、交感神经系统激活,以及随后免疫功能的变化。长期暴露于压力会破坏神经内分泌系统和免疫系统之间的稳态通信,使免疫信号转向促炎状态。压力诱导的慢性低度炎症和免疫监视功能下降都与癌症的发生和发展有关。相反,肿瘤诱导的炎性细胞因子除了驱动支持肿瘤的炎性微环境外,还可通过血液循环在远处发挥其生物学作用,从而对压力反应产生不利影响。在这篇综述中,我们总结了目前关于压力与癌症关系的研究结果,重点关注炎症在压力诱导的神经内分泌-免疫相互作用中的作用。我们还讨论了潜在机制及其在癌症治疗和预防中的潜力。