PMID- 25051397
OWN - NLM
STAT- MEDLINE
DCOM- 20150522
LR  - 20220316
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 10
IP  - 4
DP  - 2014 Oct
TI  - Effect of ginsenoside Rh2 on the migratory ability of HepG2 liver carcinoma 
      cells: recruiting histone deacetylase and inhibiting activator protein 1 
      transcription factors.
PG  - 1779-85
LID - 10.3892/mmr.2014.2392 [doi]
AB  - In previous experiments, ginsenoside Rh2 induced apoptosis and cell cycle arrest, 
      which indicates a potential role for ginsenoside Rh2 in anticancer treatment. The 
      effect of ginsenoside Rh2 on cancer is marked and ginsenoside Rh2 has been shown 
      to inhibit pancreatic tumor migratory ability. In the present study, Transwell 
      chambers were used in order to investigate whether ginsenoside Rh2 inhibits the 
      migratory ability of HepG2 liver carcinoma cells. Furthermore, to analyze 
      activator protein 1 (AP-1) transcription factor expression following Rh2 
      treatment, ten plasmids encoding Renilla luciferase coupled to the transcription 
      factors were transiently transfected into the HepG2 cells and luciferase was 
      detected by the Luciferase Reporter Assay system reagent. The results indicated 
      that ginsenoside Rh2 inhibited HepG2 cell migratory ability. The expression 
      levels of AP-1 transcription factors were increased in HepG2 cells following 
      induction by phorbol 12-myristate 13-acetate, but ginsenoside Rh2 suppressed this 
      induced AP‑1 expression. AP-1 transcription factors recruit histone deacetylase 
      (HDAC)4 and affect its transcription, thus, the expression levels of HDAC4 were 
      also analyzed, and these were found to be increased in the Rh2 treatment group. 
      Matrix metalloproteinase 3 (MMP3), a gene downstream of AP-1, was then 
      investigated, and the treatment group expressed reduced levels of MMP3 gene and 
      protein. Therefore, the inhibitory effect of ginsenoside Rh2 on the migratory 
      ability of HepG2 may be presumed to occur by the recruitment of HDAC and the 
      resulting inhibition of AP‑1 transcription factors, in order to reduce the 
      expression levels of MMP3 gene and protein.
FAU - Shi, Qingqiang
AU  - Shi Q
AD  - Laboratory of Stem Cell and Tissue Engineering, Department of Histology and 
      Embryology, Chongqing Medical University, Chongqing 40016, P.R. China.
FAU - Li, Jing
AU  - Li J
AD  - Laboratory of Stem Cell and Tissue Engineering, Department of Histology and 
      Embryology, Chongqing Medical University, Chongqing 40016, P.R. China.
FAU - Feng, Ziqiang
AU  - Feng Z
AD  - Laboratory of Stem Cell and Tissue Engineering, Department of Histology and 
      Embryology, Chongqing Medical University, Chongqing 40016, P.R. China.
FAU - Zhao, Lvcui
AU  - Zhao L
AD  - Laboratory of Stem Cell and Tissue Engineering, Department of Histology and 
      Embryology, Chongqing Medical University, Chongqing 40016, P.R. China.
FAU - Luo, Lian
AU  - Luo L
AD  - Laboratory of Stem Cell and Tissue Engineering, Department of Histology and 
      Embryology, Chongqing Medical University, Chongqing 40016, P.R. China.
FAU - You, Zhimei
AU  - You Z
AD  - Laboratory of Stem Cell and Tissue Engineering, Department of Histology and 
      Embryology, Chongqing Medical University, Chongqing 40016, P.R. China.
FAU - Li, Danyang
AU  - Li D
AD  - Laboratory of Stem Cell and Tissue Engineering, Department of Histology and 
      Embryology, Chongqing Medical University, Chongqing 40016, P.R. China.
FAU - Xia, Jing
AU  - Xia J
AD  - Laboratory of Stem Cell and Tissue Engineering, Department of Histology and 
      Embryology, Chongqing Medical University, Chongqing 40016, P.R. China.
FAU - Zuo, Guowei
AU  - Zuo G
AD  - Laboratory of Clinical Diagnostics, Chongqing Medical University, Chongqing 
      40016, P.R. China.
FAU - Chen, Dilong
AU  - Chen D
AD  - Laboratory of Stem Cell and Tissue Engineering, Department of Histology and 
      Embryology, Chongqing Medical University, Chongqing 40016, P.R. China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140718
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Ginsenosides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Repressor Proteins)
RN  - 0 (Transcription Factor AP-1)
RN  - 57716-89-9 (4-O-methyl-12-O-tetradecanoylphorbol 13-acetate)
RN  - 78214-33-2 (ginsenoside Rh2)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
RN  - EC 3.5.1.98 (HDAC4 protein, human)
RN  - EC 3.5.1.98 (Histone Deacetylases)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Cell Movement/*drug effects
MH  - Down-Regulation/drug effects
MH  - Ginsenosides/*toxicity
MH  - Hep G2 Cells
MH  - Histone Deacetylases/genetics/metabolism
MH  - Humans
MH  - Liver Neoplasms/metabolism/pathology
MH  - Matrix Metalloproteinase 3/genetics/metabolism
MH  - RNA, Messenger/metabolism
MH  - Repressor Proteins/genetics/metabolism
MH  - Tetradecanoylphorbol Acetate/analogs & derivatives/pharmacology
MH  - Transcription Factor AP-1/antagonists & inhibitors/genetics/*metabolism
PMC - PMC4148366
EDAT- 2014/07/23 06:00
MHDA- 2015/05/23 06:00
PMCR- 2014/07/18
CRDT- 2014/07/23 06:00
PHST- 2014/03/05 00:00 [received]
PHST- 2014/06/24 00:00 [accepted]
PHST- 2014/07/23 06:00 [entrez]
PHST- 2014/07/23 06:00 [pubmed]
PHST- 2015/05/23 06:00 [medline]
PHST- 2014/07/18 00:00 [pmc-release]
AID - mmr-10-04-1779 [pii]
AID - 10.3892/mmr.2014.2392 [doi]
PST - ppublish
SO  - Mol Med Rep. 2014 Oct;10(4):1779-85. doi: 10.3892/mmr.2014.2392. Epub 2014 Jul 
      18.