http://dx.doi.org/10.1016/j.lfs.2011.04.007">
 

Document Type

Journal Article

Department/Unit

School of Chinese Medicine

Title

Effects of adrenaline in human colon adenocarcinoma HT-29 cells

Language

English

Abstract

Aims: Stress has been implicated in the development of cancers. Adrenaline levels are increased in response to stress. The effects of adrenaline on colon cancer are largely unknown. The aims of the study are to determine the effects of adrenaline in human colon adenocarcinoma HT-29 cells and the possible underlying mechanisms involved. Main methods: The effect of adrenaline on HT-29 cell proliferation was determined by [3H] thymidine incorporation assay. Expression of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) were detected by Western blot. Matrix metalloproteinase-9 (MMP-9) activity and prostaglandin E2 (PGE2) release were determined by zymography and enzyme immunoassay, respectively. Key findings: Adrenaline stimulated HT-29 cell proliferation. This was accompanied by the enhanced expression of COX-2 and VEGF in HT-29 cells. Adrenaline also upregulated MMP-9 activity and PGE2 release. Adrenaline stimulated HT-29 cell proliferation which was reversed by COX-2 inhibitor sc-236. COX-2 inhibitor also reverted the action of adrenaline on VEGF expression and MMP-9 activity. Further study was performed to determine the involvement of β-adrenoceptors. The stimulatory action of adrenaline on colon cancer growth was blocked by atenolol and ICI 118,551, a β1- and β2-selective antagonist, respectively. This signified the role of β-adrenoceptors in this process. In addition, both antagonists also abrogated the stimulating actions of adrenaline on COX-2, VEGF expression, MMP-9 activity and PGE2 release in HT-29 cells. Significance: These results suggest that adrenaline stimulates cell proliferation of HT-29 cells via both β1- and β2-adrenoceptors by a COX-2 dependent pathway. © 2011 Elsevier Inc. All rights reserved.

Keywords

Adrenaline, Colon cancer, COX-2, Stress

Publication Date

2011

Source Publication Title

Life Sciences

Volume

88

Issue

25-26

Start Page

1108

End Page

1112

Publisher

Elsevier

ISSN (print)

00243205

ISSN (electronic)

18790631

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