Department of Infectious Diseases‑COVID‑19 Unit, Laiko General Hospital, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece.
Unit of Endocrinology, First Department of Internal Medicine, Laiko General Hospital, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece.
Int J Oncol. 2023 Nov;63(5). doi: 10.3892/ijo.2023.5572. Epub 2023 Sep 15.
Stress is a state of disrupted homeostasis, triggered by intrinsic or extrinsic factors, the stressors, which are counteracted by various physiological and behavioural adaptive responses. Stress has been linked to cancer development and incidence for decades; however, epidemiological studies and clinical trials have yielded contradictory results. The present review discusses the effects of stress on cancer development and the various underlying mechanisms. Animal studies have revealed a clear link between stress and cancer progression, revealing molecular, cellular and endocrine processes that are implicated in these effects. Thus, stress hormones, their receptor systems and their intracellular molecular pathways mediate the effects of stress on cancer initiation, progression and the development of metastases. The mechanisms linking stress and cancer progression can either be indirect, mediated by changes in the cancer microenvironment or immune system dysregulation, or direct, through the binding of neuroendocrine stress‑related signalling molecules to cancer cell receptors. Stress affects numerous anti‑ and pro‑cancer immune system components, including host resistance to metastasis, tumour retention and/or immune suppression. Chronic psychological stress through the elevation of catecholamine levels may increase cancer cell death resistance. On the whole, stress is linked to cancer development and incidence, with psychological stressors playing a crucial role. Animal studies have revealed a better link than human ones, with stress‑related hormones influencing tumour development, migration, invasion and cell proliferation. Randomized controlled trials are required to further evaluate the long‑term cancer outcomes of stress and its management.
压力是一种内稳态失调的状态,由内在或外在因素(应激源)引发,而各种生理和行为适应性反应则会对抗这些应激源。几十年来,压力一直与癌症的发生和发展有关;然而,流行病学研究和临床试验得出了相互矛盾的结果。本综述讨论了压力对癌症发展的影响以及各种潜在的机制。动物研究清楚地表明了压力与癌症进展之间存在联系,揭示了涉及这些影响的分子、细胞和内分泌过程。因此,应激激素、它们的受体系统及其细胞内分子途径介导了压力对癌症发生、进展和转移发展的影响。将压力与癌症进展联系起来的机制既可以是间接的,通过癌症微环境或免疫系统失调的变化介导,也可以是直接的,通过神经内分泌应激相关信号分子与癌细胞受体的结合。压力会影响许多抗癌和促癌免疫系统成分,包括宿主对转移、肿瘤保留和/或免疫抑制的抵抗力。通过儿茶酚胺水平升高引起的慢性心理压力可能会增加癌细胞的死亡抵抗能力。总的来说,压力与癌症的发生和发展有关,心理应激源起着至关重要的作用。动物研究比人类研究揭示出了更好的联系,应激相关激素会影响肿瘤的发展、迁移、侵袭和细胞增殖。需要进行随机对照试验来进一步评估压力及其管理对长期癌症结局的影响。