PMID- 31347168
OWN - NLM
STAT- MEDLINE
DCOM- 20201016
LR  - 20201016
IS  - 1097-4652 (Electronic)
IS  - 0021-9541 (Linking)
VI  - 235
IP  - 2
DP  - 2020 Feb
TI  - Glycochenodeoxycholate promotes the metastasis of gallbladder cancer cells by 
      inducing epithelial to mesenchymal transition via activation of SOCS3/JAK2/STAT3 
      signaling pathway.
PG  - 1615-1623
LID - 10.1002/jcp.29080 [doi]
AB  - The incidence of gallbladder cancer (GBC) is relatively rare but a high degree of 
      malignancy. The migration and invasion potential of GBC severely affects the 
      prognosis of patients with GBC. Glycochenodeoxycholate (GCDC) is one of the most 
      important components in GBC-associated microenvironment. However, the role of 
      GCDC in the metastatic feature of GBC cells is not fully understood. First, the 
      results of this study found that GCDC could effectively enhance the metastasis of 
      GBC cells. Furthermore, GCDC could lead to the enhancement of epithelial to 
      mesenchymal transition (EMT) phenotype in GBC cells, which is concerned to be an 
      important mechanism of tumor metastasis. Further studies showed that GCDC 
      treatment induced the upregulation of matrix metalloproteinase-3 (MMP3), MMP9, 
      and SOCS3/JAK2/p-STAT3 signal pathway in GBC cells, which could regulate the 
      level of EMT. Beside that, we also found the positive expression of farnesoid X 
      receptor (FXR) in GBC cells and inhibition of FXR could significantly block the 
      effect of GCDC on the metastasis of GBC cells. These results indicated that GCDC 
      promoted GBC cells metastasis by enhancing the level of EMT and inhibition of FXR 
      could significantly block the effect of GCDC. On one hand, FXR might be an 
      indicator for predicting the metastasis of patient with GBC. On the other hand, 
      FXR might serve as a potential antimetastasis target in GBC therapy.
CI  - (c) 2019 Wiley Periodicals, Inc.
FAU - Wang, Hui
AU  - Wang H
AD  - Department of Biliary-Pancreatic Surgery, Renji Hospital, School of Medicine, 
      Shanghai Jiao Tong University, Shanghai, P.R. China.
FAU - Zhan, Ming
AU  - Zhan M
AD  - Department of Biliary-Pancreatic Surgery, Renji Hospital, School of Medicine, 
      Shanghai Jiao Tong University, Shanghai, P.R. China.
FAU - Liu, Qiang
AU  - Liu Q
AD  - Department of Pathology, Renji Hospital, School of Medicine, Shanghai Jiao Tong 
      University, Shanghai, P.R. China.
FAU - Wang, Jian
AU  - Wang J
AUID- ORCID: 0000-0002-9974-5242
AD  - Department of Biliary-Pancreatic Surgery, Renji Hospital, School of Medicine, 
      Shanghai Jiao Tong University, Shanghai, P.R. China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190725
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (SOCS3 protein, human)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (STAT3 protein, human)
RN  - 0 (Suppressor of Cytokine Signaling 3 Protein)
RN  - 640-79-9 (Glycochenodeoxycholic Acid)
RN  - EC 2.7.10.2 (JAK2 protein, human)
RN  - EC 2.7.10.2 (Janus Kinase 2)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
SB  - IM
MH  - Animals
MH  - Cell Line, Tumor
MH  - Epithelial-Mesenchymal Transition/*drug effects
MH  - *Gallbladder Neoplasms
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Glycochenodeoxycholic Acid/*pharmacology
MH  - Humans
MH  - Janus Kinase 2/genetics/metabolism
MH  - Matrix Metalloproteinase 3/genetics/metabolism
MH  - Matrix Metalloproteinase 9/genetics/metabolism
MH  - Mice
MH  - Mice, Nude
MH  - *Neoplasm Metastasis
MH  - Neoplasms, Experimental
MH  - STAT3 Transcription Factor/genetics/metabolism
MH  - Signal Transduction
MH  - Suppressor of Cytokine Signaling 3 Protein/genetics/*metabolism
MH  - Up-Regulation
OTO - NOTNLM
OT  - epithelial to mesenchymal transition
OT  - farnesoid X receptor
OT  - gallbladder cancer cells
OT  - glycochenodeoxycholate
OT  - metastasis
EDAT- 2019/07/28 06:00
MHDA- 2020/10/21 06:00
CRDT- 2019/07/27 06:00
PHST- 2018/12/01 00:00 [received]
PHST- 2019/06/13 00:00 [accepted]
PHST- 2019/07/28 06:00 [pubmed]
PHST- 2020/10/21 06:00 [medline]
PHST- 2019/07/27 06:00 [entrez]
AID - 10.1002/jcp.29080 [doi]
PST - ppublish
SO  - J Cell Physiol. 2020 Feb;235(2):1615-1623. doi: 10.1002/jcp.29080. Epub 2019 Jul 
      25.