Stress Hormones Regulate Interleukin-6 Expression by Human Ovarian Carcinoma Cells through a Src-dependent Mechanism

Nilsson, Monique B.; Armaiz-Pena, Guillermo N.; Takahashi, Rie; Lin, Yvonne G.; Treviño, José G.; Li, Yang; Jennings, Nicholas B.; Arevalo, Jesusa M.G.; Lutgendorf, Susan K.; Gallick, Gary E.; Sanguino, Ángela; López-Berestein, Gabriel; Cole, Steven W.; Sood, Anil K.

doi:10.1074/jbc.m611539200

Cited by 133 publications

(126 citation statements)

References 38 publications

(40 reference statements)

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“…IL-6 and its downstream signaling through signal transducer and activator of transcription 3 is associated with increased proliferation, survival and secretion of matrix metalloproteinases and angiogenic mediators (Nilsson et al, 2007). IL-8 exerts an effect as a downstream signaling mediator for TNF-a and lysophosphatidic acid in ovarian cancer, augmenting proliferation, angiogenesis and invasion (Abdollahi et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

TCEAL7, a putative tumor suppressor gene, negatively regulates NF-κB pathway

et al. 2009

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Section: Discussionmentioning

confidence: 99%

TCEAL7, a putative tumor suppressor gene, negatively regulates NF-κB pathway

et al. 2009

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“…Significant increases in IL-6 promoter activity were also observed indicating that catecholamines regulate the IL-6 gene at the transcriptional level. The effects of norepinephrine on IL-6 production in ovarian carcinoma cells were found to be mediated through a β-adrenergic receptor/Src tyrosine kinase axis [55].…”

Section: Angiogenesismentioning

confidence: 98%

Neuroendocrine influences on cancer biology

Thaker

Sood

2008

Seminars in Cancer Biology

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Over the past 25 years, epidemiological and clinical studies have linked psychological factors such as stress, chronic depression, and lack of social support to the incidence and progression of cancer [1,2]. Although the mechanisms underlying these observations are not completely understood, recent molecular and animal studies have begun to identify specific signaling pathways that could explain the impact of neuroendocrine effects on tumor growth and metastasis. This review will highlight the importance of known clinical, molecular, and cellular processes with regard to the neuroendocrine stress effects on tumor biology and discuss possible behavioral and pharmacological interventions to ameliorate these effects and ultimately improve cancer outcomes.

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“…A simple time course is that while a high level of NE is excessively stimulating its receptors on a cell, this increases the probability of immediately developing cancer within that cell; however, epidemiological drug studies suggest that there may be a significant delay, perhaps of many years. Molecular cancer researchers are already elucidating signaling pathways that may be affected by NE binding to its extracellular receptors, 64 such as the RAS signaling pathway 65 and the transcription factor Stat3, 66 while perhaps in most cases not considering possible influences of NE on these pathways.…”

Section: Literature Search Detailsmentioning

confidence: 99%

Is norepinephrine an etiological factor in some types of cancer?

Fitzgerald

2008

Intl Journal of Cancer

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I examine evidence that the signaling molecule norepinephrine (NE) is an etiological factor in some types of cancer. In support of this hypothesis, I cite the following 7 lines of evidence: (i) rodent studies of tumorigenesis in the context of NE manipulation; (ii) human studies of tricyclic antidepressant use and cancer rate; (iii) existence of pheochromocytoma, a cancer of the adrenal glands; (iv) cancer rate in families with individuals who have bipolar disorder; (v) hypertension and cancer risk; (vi) excessive body weight and cancer risk; and (vii) psychological stressors and cancer risk. Three aspects of the body's NE system are consistent with it playing an etiological role in various types of cancer: (i) NE circulates in the blood and can thereby access organ systems throughout the body, in addition to direct peripheral release by the sympathetic nervous system and being released within the brain; (ii) many of the body's organs possess NE receptors on the outer surface of at least some of their cells; (iii) by binding to its extracellular receptors, NE affects intracellular second messenger systems that could influence carcinogenesis. Most importantly, use of existing pharmaceutical drugs that either lower the level of NE (such as clonidine) or block NE receptors may lower the probability of an individual developing cancer, and this hypothesis could be tested immediately by an epidemiologist through examination of existing medical records. ' 2008 Wiley-Liss, Inc.Key words: norepinephrine; pharmacology; clonidine; adrenoceptor; rodent; hypertension; epidemiology; pheochromocytoma I present evidence that the signaling molecule norepinephrine (NE), which is a neurotransmitter and plays various roles in organs other than the brain, is an etiological factor in some types of cancer. In support of this hypothesis, I cite the following 7 lines of evidence: (i) in a series of rodent studies, increasing the level of NE in various organs increases tumorigenesis, whereas decreasing the level decreases tumorigenesis; (ii) in humans, tricyclic antidepressant use, which may boost the level of NE throughout the body, may be associated with increased rates of cancer; (iii) pheochromocytoma, which is a cancer of the adrenal glands, may be an example of NE causing cancer in the organ that releases it into the bloodstream; (iv) families with individuals who have bipolar disorder have elevated cancer rates, where bipolar disorder may be associated with a high level of NE; (v) hypertension is associated with an elevated level of NE in the bloodstream, and may be a cancer risk factor; (vi) excessive body weight is associated with elevated blood NE and is a cancer risk factor; and (vii) psychological stressors are associated with increased release of NE in the brain and bloodstream, and exposure to stress is potentially a cancer risk factor.In addition to the above evidence, including NE's role in the brain, several other aspects of the body's NE system are consistent with an etiological role in cancer: (i) In addition to relea...

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Stress Hormones Regulate Interleukin-6 Expression by Human Ovarian Carcinoma Cells through a Src-dependent Mechanism

Cited by 133 publications

References 38 publications

TCEAL7, a putative tumor suppressor gene, negatively regulates NF-κB pathway

TCEAL7, a putative tumor suppressor gene, negatively regulates NF-κB pathway

Neuroendocrine influences on cancer biology

Is norepinephrine an etiological factor in some types of cancer?

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