Stress, catecholaminergic system and cancer

Križanová, Oľga; Babula, Petr; Pacák, Karel

doi:10.1080/10253890.2016.1203415

Cited by 95 publications

(80 citation statements)

References 101 publications

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“…Chronic stress has been demonstrated to account for a place in physiological and pathological disease outcomes, including several types of cancers (Krizanova et al, 2016). Chronic stress is thought to correlate with the etiology of tumor growth, progression and metastasis (Thaker et al, 2006).…”

Section: Stress Inflammation and Diseasesmentioning

confidence: 99%

Inflammation: The Common Pathway of Stress-Related Diseases

Liu

Wang

Jiang

2017

Front. Hum. Neurosci.

572

333

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While modernization has dramatically increased lifespan, it has also witnessed that the nature of stress has changed dramatically. Chronic stress result failures of homeostasis thus lead to various diseases such as atherosclerosis, non-alcoholic fatty liver disease (NAFLD) and depression. However, while 75%–90% of human diseases is related to the activation of stress system, the common pathways between stress exposure and pathophysiological processes underlying disease is still debatable. Chronic inflammation is an essential component of chronic diseases. Additionally, accumulating evidence suggested that excessive inflammation plays critical roles in the pathophysiology of the stress-related diseases, yet the basis for this connection is not fully understood. Here we discuss the role of inflammation in stress-induced diseases and suggest a common pathway for stress-related diseases that is based on chronic mild inflammation. This framework highlights the fundamental impact of inflammation mechanisms and provides a new perspective on the prevention and treatment of stress-related diseases.

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Section: Stress Inflammation and Diseasesmentioning

confidence: 99%

Inflammation: The Common Pathway of Stress-Related Diseases

Liu

Wang

Jiang

2017

Front. Hum. Neurosci.

572

333

View full text Add to dashboard Cite

show abstract

“…Stress occurs when an organism perceives a disruption, or a threat of disruption, of homeostasis. Factors that can induce stress include, among others, social circumstances, physical environment, hypoxia, emotional state, pain, glucose deprivation, accidents and chronic anxiety (5). Stress-related symptoms include negative emotions or altered mood and behavior, such as anxiety, irritability, anger, startle response, hostility and depression, which can negatively affect various organs of the human body (6).…”

Section: Introductionmentioning

confidence: 99%

Mechanisms underlying the effects of stress on tumorigenesis and metastasis (Review)

Zhang

Wang

2018

Int J Oncol

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Stress is one of the fundamental survival mechanisms in nature. Although chronic or long-lasting stress can be detrimental to health, acute or short-term stress can have health benefits. The aim of the present review was to address the complexity and significance of stress in tumorigenesis. The review covers an evaluation of previously used and reported experimental animal models of stress, as well as the effects of stress on the neuroendocrine system, immune function, gut microbiota, and inflammation and multidrug resistance, all of which are closely associated with cancer occurrence, progression and treatment. The review concludes that understanding the efficacy of stress management (prevention and rehabilitation) is crucial to the development of comprehensive and individualized strategies for cancer prevention and treatment.

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“…Since disease progression on sirolimus can be variable, we examined other pathways that might be involved in LAM disease progression. The cAMP/PKA pathway, as activated by chronic stress through beta2-adrenergic receptors, may be involved in tumor progression and metastasis (33,34). A significant fraction of patients with LAM have reversible airflow obstruction that is treated with short-or long-acting bronchodilators (9).…”

mentioning

confidence: 99%

Effect of beta-agonists on LAM progression and treatment

Kang

Steagall

Stylianou

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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Lymphangioleiomyomatosis (LAM), a rare disease of women, is associated with cystic lung destruction resulting from the proliferation of abnormal smooth muscle-like LAM cells with mutations in the tuberous sclerosis complex (TSC) genes and/or The mutant genes and encoded proteins are responsible for activation of the mechanistic target of rapamycin (mTOR), which is inhibited by sirolimus (rapamycin), a drug used to treat LAM. Patients who have LAM may also be treated with bronchodilators for asthma-like symptoms due to LAM. We observed stabilization of forced expiratory volume in 1 s over time in patients receiving sirolimus and long-acting beta-agonists with short-acting rescue inhalers compared with patients receiving only sirolimus. Because beta-agonists increase cAMP and PKA activity, we investigated effects of PKA activation on the mTOR pathway. Human skin fibroblasts or LAM lung cells incubated short-term with isoproterenol (beta-agonist) showed a sirolimus-independent increase in phosphorylation of S6, a downstream effector of the mTOR pathway, and increased cell growth. Cells incubated long-term with isoproterenol, which may lead to beta-adrenergic receptor desensitization, did not show increased S6 phosphorylation. Inhibition of PKA blocked the isoproterenol effect on S6 phosphorylation. Thus, activation of PKA by beta-agonists increased phospho-S6 independent of mTOR, an effect abrogated by beta-agonist-driven receptor desensitization. In agreement, retrospective clinical data from patients with LAM suggested that a combination of bronchodilators in conjunction with sirolimus may be preferable to sirolimus alone for stabilization of pulmonary function.

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Stress, catecholaminergic system and cancer

Cited by 95 publications

References 101 publications

Inflammation: The Common Pathway of Stress-Related Diseases

Inflammation: The Common Pathway of Stress-Related Diseases

Mechanisms underlying the effects of stress on tumorigenesis and metastasis (Review)

Effect of beta-agonists on LAM progression and treatment

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