Bibliographic Details
Title: |
Glycogen synthase kinase-3β is associated with the prognosis of hepatocellular carcinoma and may mediate the influence of type 2 diabetes mellitus on hepatocellular carcinoma. |
Authors: |
Guoliang Qiao, Yuan Le, Jun Li, Lianghuan Wang, Feng Shen |
Source: |
PLoS ONE, Vol 9, Iss 8, p e105624 (2014) |
Publisher Information: |
Public Library of Science (PLoS), 2014. |
Publication Year: |
2014 |
Collection: |
LCC:Medicine LCC:Science |
Subject Terms: |
Medicine, Science |
More Details: |
BACKGROUND: Although many studies have shown glycogen synthase kinase-3β (GSK-3β) was associated with type 2 diabetes mellitus (T2DM) and implicated with a wide range of cancers, the role of GSK-3β in hepatocellular carcinoma(HCC) and the correlation among GSK-3β, T2DM and HCC remains unclear. Our objectives were to identify the effect of p-Ser9-GSK-3β on the prognosis of patients with HCC and to learn more about the interaction among T2DM, GSK-3β and the prognosis of HCC. METHODS: Firstly we used reverse transcriptase-PCR(RT-PCR) and western blotting to determine the expression levels of GSK-3β and p-Ser9-GSK-3β in human HCC samples. We then used immunohistochemical staining to evaluate the expression pattern of p-Ser9-GSK-3β in 178 patients with HCC after curative partial hepatectomy. Finally we statistically analyzed the association of p-Ser9-GSK-3β and T2DM with the prognosis of patients with HCC. RESULTS: P-Ser9-GSK-3β was over-expressed in tumor tissues compared with their normal counterparts. Correlation and regression analysis indicated that the over-expression of p-Ser9-GSK-3β was significantly associated with T2DM, and the correlation coefficient was 0.259 (P = 0.001). Multivariate analysis showed that the over-expression of p-Ser9-GSK-3β(P |
Document Type: |
article |
File Description: |
electronic resource |
Language: |
English |
ISSN: |
1932-6203 |
Relation: |
http://europepmc.org/articles/PMC4144855?pdf=render; https://doaj.org/toc/1932-6203 |
DOI: |
10.1371/journal.pone.0105624 |
Access URL: |
https://doaj.org/article/a85733d1d8554ce4bb00149900fd55dd |
Accession Number: |
edsdoj.85733d1d8554ce4bb00149900fd55dd |
Database: |
Directory of Open Access Journals |