PMID- 25157753
OWN - NLM
STAT- MEDLINE
DCOM- 20150513
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 9
IP  - 8
DP  - 2014
TI  - Glycogen synthase kinase-3beta is associated with the prognosis of hepatocellular 
      carcinoma and may mediate the influence of type 2 diabetes mellitus on 
      hepatocellular carcinoma.
PG  - e105624
LID - 10.1371/journal.pone.0105624 [doi]
LID - e105624
AB  - BACKGROUND: Although many studies have shown glycogen synthase kinase-3beta (GSK-3beta) 
      was associated with type 2 diabetes mellitus (T2DM) and implicated with a wide 
      range of cancers, the role of GSK-3beta in hepatocellular carcinoma(HCC) and the 
      correlation among GSK-3beta, T2DM and HCC remains unclear. Our objectives were to 
      identify the effect of p-Ser9-GSK-3beta on the prognosis of patients with HCC and to 
      learn more about the interaction among T2DM, GSK-3beta and the prognosis of HCC. 
      METHODS: Firstly we used reverse transcriptase-PCR(RT-PCR) and western blotting 
      to determine the expression levels of GSK-3beta and p-Ser9-GSK-3beta in human HCC 
      samples. We then used immunohistochemical staining to evaluate the expression 
      pattern of p-Ser9-GSK-3beta in 178 patients with HCC after curative partial 
      hepatectomy. Finally we statistically analyzed the association of p-Ser9-GSK-3beta 
      and T2DM with the prognosis of patients with HCC. RESULTS: P-Ser9-GSK-3beta was 
      over-expressed in tumor tissues compared with their normal counterparts. 
      Correlation and regression analysis indicated that the over-expression of 
      p-Ser9-GSK-3beta 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-3beta(P<0.001) and T2DM(P = 0.008) were independently 
      associated with poor prognosis of HCC, respectively. Further analysis 
      demonstrated that these two variables are closely related with each other. 
      CONCLUSION: The over-expression of p-Ser9-GSK-3beta and T2DM are strongly correlated 
      with worse surgical outcome of HCC. P-Ser9-GSK-3beta may play a significant role in 
      mediating the influence of T2DM on the prognosis of HCC.
FAU - Qiao, Guoliang
AU  - Qiao G
AD  - Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Second 
      Military Medical University, Shanghai, China.
FAU - Le, Yuan
AU  - Le Y
AD  - Department of Biochemistry and Molecular Biology, Second Military Medical 
      University, Shanghai, China.
FAU - Li, Jun
AU  - Li J
AD  - Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Second 
      Military Medical University, Shanghai, China.
FAU - Wang, Lianghuan
AU  - Wang L
AD  - Department of Biochemistry and Molecular Biology, Second Military Medical 
      University, Shanghai, China.
FAU - Shen, Feng
AU  - Shen F
AD  - Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Second 
      Military Medical University, Shanghai, China.
LA  - eng
PT  - Journal Article
DEP - 20140826
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (RNA, Messenger)
RN  - EC 2.7.11.26 (Glycogen Synthase Kinase 3)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Carcinoma, Hepatocellular/*complications/*diagnosis/genetics/surgery
MH  - Diabetes Mellitus, Type 2/*complications/*enzymology/genetics
MH  - Female
MH  - Glycogen Synthase Kinase 3/analysis/*genetics
MH  - Hepatectomy
MH  - Humans
MH  - Liver/enzymology/pathology/surgery
MH  - Liver Neoplasms/*complications/*diagnosis/genetics/surgery
MH  - Male
MH  - Middle Aged
MH  - Prognosis
MH  - RNA, Messenger/genetics
MH  - Treatment Outcome
MH  - Up-Regulation
MH  - Young Adult
PMC - PMC4144855
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2014/08/27 06:00
MHDA- 2015/05/15 06:00
PMCR- 2014/08/26
CRDT- 2014/08/27 06:00
PHST- 2014/05/28 00:00 [received]
PHST- 2014/07/22 00:00 [accepted]
PHST- 2014/08/27 06:00 [entrez]
PHST- 2014/08/27 06:00 [pubmed]
PHST- 2015/05/15 06:00 [medline]
PHST- 2014/08/26 00:00 [pmc-release]
AID - PONE-D-14-23878 [pii]
AID - 10.1371/journal.pone.0105624 [doi]
PST - epublish
SO  - PLoS One. 2014 Aug 26;9(8):e105624. doi: 10.1371/journal.pone.0105624. 
      eCollection 2014.