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Psychological Stress Up-Regulates CD147 Expression Through Beta-Arrestin1/ERK to Promote Proliferation and Invasiveness of Glioma Cells. Wang Ping,Wang Zhenming,Yan Yizhi,Xiao Lin,Tian Wenxiu,Qu Meihua,Meng Aixia,Sun Fengxiang,Li Guizhi,Dong Junhong Frontiers in oncology Psychological stress is closely related to the occurrence and prognosis of various malignant tumors, but the underlying mechanisms are not well studied. CD147 has been reported to be expressed in glioma and other malignant tumors. CD147 not only participates in lactic acid transport, but it also plays an important role in the invasion and metastasis of malignant tumor cells by stimulating the production of numerous matrix metalloproteinases (MMPs) and vascular endothelial growth factor by fibroblasts, and could also act as an autocrine factor stimulating MMPs production in metastatic tumor cells. Here, we found that silencing CD147 in chronically stressed nude mice not only inhibited the proliferation of xenografts but also decreased matrix metalloproteinase-2, 9 expression and lactic acid content in tumor tissues. Furthermore, norepinephrine (NE) was significantly increased in the serum of nude mice in glioma stress model. To determine the underlying cellular mechanism, we added exogenous NE into LN229 and U87 cells to simulate the stress environment . The invasiveness of the glioma cells was subsequently examined using a Matrigel invasion assay. We demonstrated that knockdown of CD147 inhibited glioma invasiveness and metastasis with norepinephrine stimulation. Luciferase reporter gene experiments further demonstrated that the expression of CD147 is up-regulated primarily by norepinephrine the β-Adrenalin receptor (βAR)-β-arrestin1-ERK1/2-Sp1 pathway. High expression of CD147 promoted the secretion of MMP-2 and the increment of lactic acid, which accelerated the augmented invasion and metastasis of glioma induced by psychological stress. Taken together, these results suggest that psychological stress promotes glioma proliferation and invasiveness by up-regulating CD147 expression. Thus, CD147 might be a potential target site in the treatment of glioma progression induced by chronic psychological stress. 10.3389/fonc.2020.571181
Mechanism of chronic stress to promote tumor development and the intervention. Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences Chronic stress is a serial of non-specific neuroendocrine reactions in the body when stimulated by stressors for a long time, which has been shown to have a significant effect on tumor development. Chronic stress can activate the hypothalamus-pituitary-adrenal axis and the sense-adrenal myelin system, promote catecholamine and adrenal corticosteroid secretion, regulate the downstream pathways at all levels, and modulate the secretion of immune cells and immune factors, inhibit protective immune response, and induce inflammation, thus promoting tumor cell proliferation and metastasis. Some drugs and psychotherapy can alleviate the patient's stress state, block the nerve signal transmission at all levels of access, regulate the immune system, or can become an effective means to intervene in chronic stress in tumor patients for clinical treatment to provide reference for intervention ideas. However, due to lack of relevant clinical trials, the clinical intervention effect of various drugs and psychotherapy is uncertain and needs more studies to verify the effect. 10.11817/j.issn.1672-7347.2022.210589
Chronic Stress Related to Cancer Incidence, including the Role of Metabolic Syndrome Components. Cancers Epidemiological results on the link between chronic stress and cancer initiation have been inconsistent. This study examined the relation between chronic biological stress, indicated as hair cortisol (HairF) and hair cortisone (HairE), and cancer incidence, adjusting for metabolic syndrome (MetS) components. We analyzed HairF and HairE samples from 6341 participants from the population-based cohort Lifelines in 2014. A linkage with the Dutch Nationwide Pathology Databank (Palga) provided the cancer incidence from 2015 to 2021. The association between dichotomized HairF and log-transformed HairE (LogHairE) and cancer incidence was estimated using Cox regression. MetS components were evaluated as confounders or moderators. Of the 2776 participants with known HairF levels and no cancer history, 238 developed cancer. The HairF level did not predict cancer incidence (HR: 0.993, 95%CI: 0.740-1.333). No confounders or moderators were identified. Among the 4699 participants with known HairE levels and no cancer history, 408 developed cancer. There was no association between LogHairE and cancer incidence (HR: 1.113, 95%CI: 0.738-1.678). When including age as a confounder and gender as a moderator, LogHairE was statistically significantly associated with cancer incidence (HR: 6.403, 95%CI: 1.110-36.92). In a population-based cohort, chronic biological stress, measured by HairE, was associated with cancer incidence, after controlling for age and gender. 10.3390/cancers16112044
Molecular evaluation of chronic restrain stress in mice model of non metastatic fibrosarcoma. Journal of molecular histology Chronic stress is regarded as a significant factor in the etiology of the many diseases. Numerous methods have been developed through which the effect of chronic stress is examined. The aim of this study is to demonstrate the new experimental model for analysis of immuno-suppression induced by chronic restraint stress, through challenge with conditionally tumorigenic cell line BHK-21/C13. 20 male NMRI mice were randomly divided into 2 groups-control and experimental. Each mouse was subcutaneously inoculated with BHK-21/C13 cells. Stress in the experimental group was induced for 20 days. After the experiment, tumor masses were removed, and analyzed using histology and immunohistochemistry techniques. We found a statistically significant difference (p = 0.034) in tumor expression and tumor volumes (p = 0.0061) between groups, as well as in immunopositivity on Ki67, cytochrome C and matrix metalloproteinase 9. Absence of immune infiltrate was noticed in experimental, and the presence of inflammatory infiltrate at tumor invasion front in control group. 10.1007/s10735-020-09886-5
Chronic Stress Effects on Tumor: Pathway and Mechanism. Hong Hanqing,Ji Min,Lai Dongmei Frontiers in oncology Chronic stress is an emotional experience that occurs when people encounter something they cannot adapt to. Repeated chronic stress increases the risk of a variety of diseases, such as cardiovascular disease, depression, endocrine disease, inflammation and cancer. A growing body of research has shown that there is a link between chronic stress and tumor occurrence in both animal studies and clinical studies. Chronic stress activates the neuroendocrine system (hypothalamic-pituitary-adrenal axis) and sympathetic nervous system. Stress hormones promote the occurrence and development of tumors through various mechanisms. In addition, chronic stress also affects the immune function of the body, leading to the decline of immune monitoring ability and promote the occurrence of tumors. The mechanisms of chronic stress leading to tumor include inflammation, autophagy and epigenetics. These factors increase the proliferation and invasion capacity of tumor cells and alter the tumor microenvironment. Antagonists targeting adrenergic receptors have played a beneficial role in improving antitumor activity, as well as chemotherapy resistance and radiation resistance. Here, we review how these mechanisms contribute to tumor initiation and progression, and discuss whether these molecular mechanisms might be an ideal target to treat tumor. 10.3389/fonc.2021.738252
Chronic Stress Promotes Cancer Development. Dai Shirui,Mo Yongzhen,Wang Yumin,Xiang Bo,Liao Qianjin,Zhou Ming,Li Xiaoling,Li Yong,Xiong Wei,Li Guiyuan,Guo Can,Zeng Zhaoyang Frontiers in oncology Stress is an inevitable part of life. Chronic stress on account of reasons like adversity, depression, anxiety, or loneliness/social isolation can endanger human health. Recent studies have shown that chronic stress can induce tumorigenesis and promote cancer development. This review describes the latest progress of research on the molecular mechanisms by which chronic stress promotes cancer development. Primarily, chronic stress activates the classic neuroendocrine system [the hypothalamic-pituitary-adrenal (HPA) axis] and the sympathetic nervous system (SNS) and leads to a decline and dysfunction of the prefrontal cortex and the hippocampus under stress. Stress hormones produced during the activation of both the HPA axis and the SNS can promote tumorigenesis and cancer development through a variety of mechanisms. Chronic stress can also cause corresponding changes in the body's immune function and inflammatory response, which is significant because a long-term inflammatory response and the decline of the body's immune surveillance capabilities are implicated in tumorigenesis. Stress management is essential for both healthy people and cancer patients. Whether drugs that limit the signaling pathways downstream of the HPA axis or the SNS can suppress chronic stress-induced cancers or prolong patient survival deserves further study. 10.3389/fonc.2020.01492