PMID- 24966916
OWN - NLM
STAT- MEDLINE
DCOM- 20150223
LR  - 20211021
IS  - 1936-2625 (Electronic)
IS  - 1936-2625 (Linking)
VI  - 7
IP  - 5
DP  - 2014
TI  - Glo1 genetic amplification as a potential therapeutic target in hepatocellular 
      carcinoma.
PG  - 2079-90
AB  - Glyoxalase 1 (Glo1) gene aberrations is associated with tumorigenesis and 
      progression in numerous cancers. In this study, we explored the role of Glo1 
      genetic amplification and expression in Chinese patients with hepatocellular 
      carcinoma (HCC), and Glo1 genetic amplification as potential therapeutic target 
      for HCC. We used fluorescence in situ hybridization (FISH) analysis and qRT-PCR 
      to examine Glo1 genetic aberrations and Glo1 mRNA expression in paired tumor 
      samples obtained from HCC patients. Glo1 genetic amplification was identified in 
      a subset of HCC patient (6%, 3/50), and up-regulation of Glo1 expression was 
      found in 48% (24/50) of tumor tissues compared with adjacent non-tumorous 
      tissues. Statistic analysis showed that Glo1-upregulation significantly 
      correlated with high serum level of alpha-fetoprotein (AFP). Interfering Glo1 
      expression with shRNA knocking-down led to significant inhibition of cell growth 
      and induced apoptosis in primarily cultured HCC cells carrying genetic amplified 
      Glo1 gene, while no inhibitory effects on cell proliferation were observed in HCC 
      cells with normal copies of Glo1 gene. Glo1 knockdown also inhibited tumor growth 
      and induced apoptosis in xenograft tumors established from primarily cultured HCC 
      cells with Glo1 gene amplification. In addition, Glo1 knocking-down with shRNA 
      interfering caused cellular accumulation of methylglyoxal, a Glo1 cytotoxic 
      substrate. Our data suggested Glo1 pathway activation is required for cell 
      proliferation and cell survival of HCC cells carrying Glo1 genetic amplification. 
      Intervention of Glo1 activation could be a potential therapeutic option for 
      patients with HCC carrying Glo1 gene amplification.
FAU - Zhang, Shirong
AU  - Zhang S
AD  - Department of Oncology, Hangzhou First People's Hospital Hangzhou, Zhejiang, 
      China.
FAU - Liang, Xiaodong
AU  - Liang X
AD  - Department of Oncology, Hangzhou First People's Hospital Hangzhou, Zhejiang, 
      China.
FAU - Zheng, Xiaoliang
AU  - Zheng X
AD  - Centre of Molecular Medicine, Zhejiang Academy of Medical Sciences Hangzhou, 
      Zhejiang, China.
FAU - Huang, Haixiu
AU  - Huang H
AD  - Department of Oncology, Hangzhou First People's Hospital Hangzhou, Zhejiang, 
      China.
FAU - Chen, Xufeng
AU  - Chen X
AD  - Department of Pathology and Laboratory Medicine, University of California at Los 
      Angeles Los Angeles, CA, USA.
FAU - Wu, Kan
AU  - Wu K
AD  - Centre of Molecular Medicine, Zhejiang Academy of Medical Sciences Hangzhou, 
      Zhejiang, China.
FAU - Wang, Bing
AU  - Wang B
AD  - Centre of Molecular Medicine, Zhejiang Academy of Medical Sciences Hangzhou, 
      Zhejiang, China.
FAU - Ma, Shenglin
AU  - Ma S
AD  - Department of Oncology, Hangzhou First People's Hospital Hangzhou, Zhejiang, 
      China.
LA  - eng
PT  - Journal Article
DEP - 20140415
PL  - United States
TA  - Int J Clin Exp Pathol
JT  - International journal of clinical and experimental pathology
JID - 101480565
RN  - 0 (AFP protein, human)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (RNA, Messenger)
RN  - 0 (alpha-Fetoproteins)
RN  - 722KLD7415 (Pyruvaldehyde)
RN  - EC 4.4.1.5 (Lactoylglutathione Lyase)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Biomarkers, Tumor/*genetics/metabolism
MH  - Carcinoma, Hepatocellular/enzymology/*genetics/pathology/therapy
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - China
MH  - Female
MH  - *Gene Amplification
MH  - Gene Expression Regulation, Enzymologic
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Lactoylglutathione Lyase/*genetics/metabolism
MH  - Liver Neoplasms/enzymology/*genetics/pathology/therapy
MH  - Male
MH  - Mice, Inbred BALB C
MH  - Mice, Nude
MH  - Middle Aged
MH  - Pyruvaldehyde/metabolism
MH  - RNA Interference
MH  - RNA, Messenger/genetics
MH  - Time Factors
MH  - Transfection
MH  - Tumor Burden
MH  - Tumor Cells, Cultured
MH  - alpha-Fetoproteins/analysis
PMC - PMC4069890
OTO - NOTNLM
OT  - Glyoxalase 1
OT  - apoptosis
OT  - cell proliferation
OT  - genetic amplification
OT  - hepatocellular carcinoma
EDAT- 2014/06/27 06:00
MHDA- 2015/02/24 06:00
PMCR- 2014/04/15
CRDT- 2014/06/27 06:00
PHST- 2014/03/18 00:00 [received]
PHST- 2014/04/10 00:00 [accepted]
PHST- 2014/06/27 06:00 [entrez]
PHST- 2014/06/27 06:00 [pubmed]
PHST- 2015/02/24 06:00 [medline]
PHST- 2014/04/15 00:00 [pmc-release]
PST - epublish
SO  - Int J Clin Exp Pathol. 2014 Apr 15;7(5):2079-90. eCollection 2014.