Depression, social support, and beta-adrenergic transcription control in human ovarian cancer

Abstract Motivated by previous indications that beta-adrenergic signaling can regulate tumor cell gene expression in model systems, we sought to determine whether similar dynamics occur in primary human ovarian cancer. DNA microarray analyses of 10 ovarian carcinomas identified 266 human transcripts...

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Bibliographic Details
Published in:Brain, behavior, and immunity behavior, and immunity, 2009-02, Vol.23 (2), p.176-183
Main Authors: Lutgendorf, Susan K, DeGeest, Koen, Sung, Caroline Y, Arevalo, Jesusa M, Penedo, Frank, Lucci, Joseph, Goodheart, Michael, Lubaroff, David, Farley, Donna M, Sood, Anil K, Cole, Steve W
Format: Article
Language:English
Subjects:
Activating Transcription Factors - genetics
Activating Transcription Factors - metabolism
Adult
Aged
Aged, 80 and over
Allergy and Immunology
Beta-adrenergic receptor
Chromatography, High Pressure Liquid
Cyclic AMP Response Element-Binding Protein - genetics
Cyclic AMP Response Element-Binding Protein - metabolism
Depression - etiology
Depression - genetics
Depression - physiopathology
Female
Gene expression
Gene Expression Regulation, Neoplastic
Humans
Middle Aged
Neoplasms - metabolism
NF-kappa B - genetics
NF-kappa B - metabolism
Norepinephrine - blood
Oligonucleotide Array Sequence Analysis
Ovarian cancer
Ovarian Neoplasms - genetics
Ovarian Neoplasms - physiopathology
Ovarian Neoplasms - psychology
Psychiatry
Reverse Transcriptase Polymerase Chain Reaction
Risk Factors
Social Support
Sympathetic nervous system
Transcription factor
Transcription, Genetic
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Summary:Abstract Motivated by previous indications that beta-adrenergic signaling can regulate tumor cell gene expression in model systems, we sought to determine whether similar dynamics occur in primary human ovarian cancer. DNA microarray analyses of 10 ovarian carcinomas identified 266 human transcripts that were differentially expressed in tumors from patients with elevated biobehavioral risk factors (high depressive symptoms and low social support) relative to grade- and stage-matched tumors from low-risk patients. Promoter-based bioinformatic analyses indicated increased activity of several beta-adrenergically-linked transcription control pathways, including CREB/ATF, NF-κB/Rel, STAT, and Ets family transcription factors. Consistent with increased beta-adrenergic signaling, high biobehavioral risk patients also showed increased intra-tumor concentrations of norepinephrine (but no difference in plasma norepinephrine). These data show that genome-wide transcriptional profiles are significantly altered in tumors from patients with high behavioral risk profiles, and they identify beta-adrenergic signal transduction as a likely mediator of those effects.
ISSN:0889-1591
1090-2139
DOI:10.1016/j.bbi.2008.04.155