Social stress, coping strategies and tumor development in male mice: Behavioral, neuroendocrine and immunological implications

Vegas, Oscar; Fano, Eduardo; Brain, Paul F.; Alonso, Ana; Azpı́roz, Arantza

doi:10.1016/j.psyneuen.2005.05.013

Cited by 37 publications

(29 citation statements)

References 58 publications

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“…10 This seems to be true also for melanoma at least in in vivo models. 32,33 Our work provides evidence that stress hormones like NE and E can significantly stimulate the malignancy of melanoma cells at various levels and that b-ARs, likely involved in this response, are largely expressed in melanoma cell lines and cutaneous melanomas. It is the first time, to our knowledge, that b-ARs are demonstrated in a large series of human cutaneous melanocytic lesions, and even in melanocytic naevi, suggesting a potential influence of catecholamines also in benign counterparts.…”

Section: Discussionmentioning

confidence: 77%

β-adrenoceptors are upregulated in human melanoma and their activation releases pro-tumorigenic cytokines and metalloproteases in melanoma cell lines

Moretti

Massi

Farini

et al. 2013

Laboratory Investigation

112

108

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Recent studies sight b-adrenergic receptor (AR) antagonists as novel therapeutic agents for melanoma, as they may reduce disease progression. Here within, we evaluated the expression of b-ARs in a series of human cutaneous melanocytic lesions, and studied the effect of their endogenous agonists, norepinephrine (NE) and epinephrine (E), on primary and metastatic human melanoma cell lines. Using immunohistochemistry, we found that both b1-and b2-ARs are expressed in tissues from benign melanocytic naevi, atypical naevi and malignant melanomas and that expression was significantly higher in malignant tumours. Melanoma cell lines (human A375 primary melanoma cell line and human Hs29-4T metastatic melanoma cell lines) also expressed b1-and b2-ARs by measuring transcripts and proteins. NE or E increased metalloprotease-dependent motility, released interleukin-6 and 8 (IL-6, IL-8) and vascular endothelial growth factor (VEGF). These effects of catecholamines were inhibited by the unselective b-AR antagonist propranolol. The role of soluble factors elicited by catecholamines seemed pleiotropic as VEGF synergized with NE increased melanoma invasiveness through 3D barriers, while IL-6 participated in stromal fibroblast activation towards a myofibroblastic phenotype. Our results indicate that NE and E produce in vitro via b-ARs activation a number of biological responses that may exert a pro-tumorigenic effect in melanoma cell lines. The observation that b-ARs are upregulated in malignant melanoma tissues support the hypothesis that circulating catecholamines NE and E, by activating their receptors, favour melanoma progression in vivo. Melanoma represents the most aggressive type of skin cancer, with an increasing incidence found especially in young adults. A significant reduction in mortality has been not observed, despite a noteworthy improvement in early diagnosis achieved in recent years. 1 At present, no medical option can cure metastatic melanoma (MM) and the only effective treatment for the eradication of the disease is early-phase surgery. 2 Hence, increased knowledge of the biological pathways underlying the process of melanoma dissemination and metastasis is crucial in order to identify new therapeutic targets.Previous studies have shown that various human solid tumours, such as breast, colon, prostatic, ovary, nasopharyngeal and oral cancer, express b2-adrenoceptor (b2-AR), raising the possibility that such receptors may affect invasion and dissemination processes. [3][4][5][6][7][8] Moreover, some stress neurotransmitters, such as norepinephrine (NE) and epinephrine (E), have been demonstrated to contribute to the regulation of tumour cell invasion, at least in part through b-AR activation. 6,7,9 Interactions between tumour cells and soluble factors originated from the nervous system has recently been proposed to favour metastasis formation. 10 Improved survival rates have been demonstrated in mice with metastatic tumour by combined administration of b-AR antagonists. 11 In addition, recent evidence suggests a ...

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Section: Discussionmentioning

confidence: 77%

β-adrenoceptors are upregulated in human melanoma and their activation releases pro-tumorigenic cytokines and metalloproteases in melanoma cell lines

Moretti

Massi

Farini

et al. 2013

Laboratory Investigation

112

108

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“…The increase of the aggressive potential of melanoma tumor cells observed by Yang et al (2009) after the administration of NE is partly due at least to the fact that this catecholamine stimulates the production of VEGF, IL-8 and IL-6 (Yang et al, 2009). In this sense, the results obtained in our laboratory have shown that social stress reduces diverse parameters of the immune activity (proliferative response to Con-A, IL-2 and IL-12), and that this immunosuppression is accompanied by greater tumor development (Vegas et al, 2006). The data presented so far suggest that the course of melanoma tumor development may be affected by the hormones released during the stress response, either through the intervention of this response in the immune balance, or through other mechanisms capable of regulating the complex process of neoplastic development.…”

Section: The Effect Of Social Stress On Melanoma Tumor Developmentmentioning

confidence: 67%

“…An increase in B16 melanoma pulmonary metastasis development has also been observed (Fig. 2) in a mouse model for human melanoma applied to socially-stressed mice (Sa-Rocha et al, 2006;Vegas et al, 2006). The relationship of dominance/subordination which is necessarily established following social interaction between male mice has enabled researchers to observe that the stress to which the defeated or subordinate animals are subject triggers a significant increase in the development of B16 melanoma pulmonary metastasis.…”

Section: The Effect Of Social Stress On Melanoma Tumor Developmentmentioning

confidence: 74%

“…Subjects which adopt different coping strategies (active or passive coping strategies) have different HPA and SAM activation patterns (Koolhaas et al, 2007). Previous studies in our laboratory show that social stress increases the pulmonary metastatic development of B16 melanoma, and point to a greater degree of tumor development in subjects which employ a more passive coping strategy in response to stress (Vegas et al, 2006). The coping strategies for social stress were obtained from an exhaustive analysis of the complete mouse ethogram developed by Brain et al (1989), which covers 51 behavioral elements grouped into 11 broad categories: attack, threat, non-social exploration, social investigation, exploration from a distance, digging, body care, avoidance/flee, defense submission, sexual behavior and immobility.…”

Section: The Effect Of Social Stress On Melanoma Tumor Developmentmentioning

confidence: 90%

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Effects of Social Stress on Immunomodulation and Tumor Development

Vegas¹,

Garmendia²,

Arregi³

et al. 2011

Advances in Malignant Melanoma - Clinical and Research Perspectives

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“…A study into the relationships between acute social stress, immunological alterations and the development of pulmonary metastases of B16F10 melanoma has demonstrated the ability of social stress to result in increased numbers of pulmonary metastases and altered the serum level of corticosterone (8). In addition, a recent extensive study reported that chronic stress promotes tumor growth and angiogenesis in a mouse model of ovarian cancer (9).…”

Section: Discussionmentioning

confidence: 99%

NF-KappaB As a Critical Biological Link Between Psychological Stress and Breast Cancer

Yull¹

2007

PsycEXTRA Dataset

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Social stress, coping strategies and tumor development in male mice: Behavioral, neuroendocrine and immunological implications

Cited by 37 publications

References 58 publications

β-adrenoceptors are upregulated in human melanoma and their activation releases pro-tumorigenic cytokines and metalloproteases in melanoma cell lines

β-adrenoceptors are upregulated in human melanoma and their activation releases pro-tumorigenic cytokines and metalloproteases in melanoma cell lines

Effects of Social Stress on Immunomodulation and Tumor Development

NF-KappaB As a Critical Biological Link Between Psychological Stress and Breast Cancer

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