Depression, social support, and beta-adrenergic transcription control in human ovarian cancer
Adult
Aged, 80 and over
Ovarian Neoplasms
Transcription, Genetic
Depression
Reverse Transcriptase Polymerase Chain Reaction
NF-kappa B
1. No poverty
Social Support
Middle Aged
Activating Transcription Factors
3. Good health
Gene Expression Regulation, Neoplastic
Norepinephrine
03 medical and health sciences
0302 clinical medicine
Risk Factors
Neoplasms
Humans
Female
Cyclic AMP Response Element-Binding Protein
Chromatography, High Pressure Liquid
Aged
Oligonucleotide Array Sequence Analysis
DOI:
10.1016/j.bbi.2008.04.155
Publication Date:
2008-06-12T14:05:56Z
AUTHORS (11)
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-kappaB/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.
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