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Published in: Metabolic Brain Disease 1/2012

01-03-2012 | Original Paper

High level interleukin-6 in the medium of human pancreatic cancer cell culture suppresses production of neurotransmitters by PC12 cell line

Authors: Rong Li, Jian Hou, Qing Xu, Qing-Jun Liu, Yi-Jun Shen, Gary Rodin, Madeline Li

Published in: Metabolic Brain Disease | Issue 1/2012

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Abstract

It has been suggested that pancreatic cancer is associated with a greater prevalence of depression than many other cancers, but the mechanism accounting for this potential association has not yet been illustrated. In the present study, conditioned media (CM) from three pancreatic cancer cell lines and primary pancreatic cancer cells from two patients were added to culture system of differentiated pheochromocytoma cell line PC12. The release of dopamine (DA) and norepinephrine (NE) by PC12 was significantly inhibited after CM treatment (P < 0.05), similar to what happened after recombinant interleukin 6(IL-6) treatment. Furthermore, pretreatment with anti-IL-6 antibody significantly blocked the inhibitory effects of pancreatic cancer CM on DA and NE production (P < 0.05). We also demonstrated that tyrosine hydroxylase (TH), the rate-limiting enzyme for synthesis of catecholamine, was reduced after exposure to IL-6, which was accompanied by JAK-STAT3 pathway activation. Our results demonstrated that IL-6 in CM from pancreatic cancer down-regulated the production of DA and NE by PC12 cell. The possible underlying mechanisms might be decreasing TH production via activation of JAK-STAT3 signal transduction pathway. The present study might help to better understand the close relationship between pancreatic cancer and depression.
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Metadata
Title
High level interleukin-6 in the medium of human pancreatic cancer cell culture suppresses production of neurotransmitters by PC12 cell line
Authors
Rong Li
Jian Hou
Qing Xu
Qing-Jun Liu
Yi-Jun Shen
Gary Rodin
Madeline Li
Publication date
01-03-2012
Publisher
Springer US
Published in
Metabolic Brain Disease / Issue 1/2012
Print ISSN: 0885-7490
Electronic ISSN: 1573-7365
DOI
https://doi.org/10.1007/s11011-011-9270-x

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