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H2A Z regulates tumorigenesis, metastasis and sensitivity to cisplatin in
intrahepatic cholangiocarcinoma
#MMPMID29532867
Yang B
; Tong R
; Liu H
; Wu J
; Chen D
; Xue Z
; Ding C
; Zhou L
; Xie H
; Wu J
; Zheng S
Int J Oncol
2018[Apr]; 52
(4
): 1235-1245
PMID29532867
show ga
Intrahepatic cholangiocarcinoma (ICC) is a fatal, malignant tumor of the liver;
effective diagnostic biomarkers and therapeutic targets for ICC have not been
identified yet. High expression of H2A histone family member Z (H2A.Z) is a
high-risk factor for poor prognosis in patients with breast cancer and primary
hepatocellular cancer. However, the significance of H2A.Z and its expression in
ICC remains unknown. The present study demonstrated that H2A.Z is overexpressed
in ICC and expression of H2A.Z correlated with poor prognosis in patients with
ICC. H2A.Z regulated cell proliferation in vitro and in vivo via H2A.Z/S-phase
kinase-associated protein 2/p27/p21 signaling. Inhibition of H2A.Z reduced cell
proliferation and induced apoptosis in ICC. In addition, downregulation of H2AZ
reduced tumor metastasis by repressing epithelial-mesenchymal transition and
enhanced the antitumor effects of cisplatin in the treatment of ICC. Overall,
H2A.Z promoted cell proliferation and epithelial-mesenchymal transition in ICC,
suggesting that H2A.Z may be a novel biomarker and therapeutic target for ICC.
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