| Literature DB >> 28300577 |
Shengbing Zang1, Xiaojie Ma2, Yanbin Wu3, Wenwen Liu1, Haili Cheng1, Jiasi Li1, Jingfeng Liu3, Aimin Huang4.
Abstract
Prostaglandin E 2 (PGE2), which is the most abundant prostaglandin produced in hepatocellular carcinoma (HCC), may be involved in hepatocarcinogenesis. Here, the amount of PGE2 was significantly increased in HCC tissue and adjacent noncancerous tissues relative to normal liver tissue (P<.001). In addition, the expression of EP2 receptor was considerably upregulated in HCC tissue compared with the expression of EP1 (P<.05), EP3 (P<.01), and EP4 (P<.01) receptor. The expression of EP2 receptor was positively correlated with the level of PGE2 in HCC tissue (P<.001). Furthermore, PGE2 significantly increased proliferation and invasion potential of human HCC cells. However, antagonism of EP2 signaling suppressed PGE2-induced growth and invasion in human HCC cells. Taken together, upregulation of PGE2 level was associated with proliferation and invasion potential of HCC, and EP2 receptor predominately mediated the function of PGE2 in the transformation and progression of HCC.Entities:
Keywords: Antagonism; E prostanoid receptor; Hepatocellular carcinoma; Proliferation; Prostaglandin E 2 (PGE(2))
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Year: 2017 PMID： 28300577 DOI： 10.1016/j.humpath.2017.02.018
Source DB: PubMed Journal: Hum Pathol ISSN： 0046-8177 Impact factor: 3.466