55
Views
8
CrossRef citations to date
0
Altmetric
Miscellaneous

COX-2 – a target for preventing hepatic carcinoma?

, &
Pages 483-490 | Published online: 25 Feb 2005
 

Abstract

Hepatocellular carcinoma (HCC) is one of the most common reasons for malignancy-related death in Africa and Asia and is still recognised as the leading cancer in men in Taiwan. Despite enthusiastic efforts in early diagnosis, aggressive surgical treatment and application of additional nonoperative modalities, its prognosis is still dismal. This emphasises the necessity to develop new measures and strategies for its prevention. Inducible cyclooxygenease 2 (COX-2) is an immediate-early (IE) response gene and extensive studies conducted over the past few years have recognised its overexpression in several carcinomas and thus its implication in carcinogenesis. Recent studies have suggested that overexpression of COX-2 might be one of the leading factors in hepatic carcinogenesis. COX-2 can induce angiogenesis via vascular endothelial growth factor (VEGF) and prostaglandin production and can also inhibit apoptosis by inducing the antiapoptotic factor Bcl-2 as well as activating antiapoptotic signalling through Akt/PKB. Therefore, the use of selective inhibitors for the downregulation of COX-2 activity might be a target for preventing hepatic carcinoma development.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.