scholarly journals Zinc finger protein ZBTB20 is an independent prognostic marker and promotes tumor growth of human hepatocellular carcinoma by repressing FoxO1

Oncotarget ◽  
2016 ◽  
Vol 7 (12) ◽  
pp. 14336-14349 ◽  
Author(s):  
Heping Kan ◽  
Yuqi Huang ◽  
Xianghong Li ◽  
Dingli Liu ◽  
Jianjia Chen ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Growth ◽  
Prognostic Marker ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Human Hepatocellular Carcinoma ◽  
Independent Prognostic Marker ◽  
Finger Protein

scholarly journals Zinc finger protein 307 functions as a tumor-suppressor and inhibits cell proliferation by inducing apoptosis in hepatocellular carcinoma

2017 ◽  
Vol 38 (4) ◽  
pp. 2229-2236 ◽  
Author(s):  
Yonghao Liang ◽  
Qisheng Li ◽  
Keli Chen ◽  
Wen Ni ◽  
Zetao Zhan ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Tumor Suppressor ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Finger Protein

scholarly journals Overexpression of zinc finger protein 687 enhances tumorigenic capability and promotes recurrence of hepatocellular carcinoma

Oncogenesis ◽  
2017 ◽  
Vol 6 (7) ◽  
pp. e363-e363 ◽  
Author(s):  
T Zhang ◽  
Y Huang ◽  
W Liu ◽  
W Meng ◽  
H Zhao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Finger Protein

Zinc finger protein 191 inhibits hepatocellular carcinoma metastasis through discs large 1-mediated yes-associated protein inactivation

Hepatology ◽  
2016 ◽  
Vol 64 (4) ◽  
pp. 1148-1162 ◽  
Author(s):  
Di Wu ◽  
Guoyuan Liu ◽  
Yufeng Liu ◽  
Hexige Saiyin ◽  
Chenji Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Protein Inactivation ◽  
Finger Protein ◽  
Discs Large ◽  
Carcinoma Metastasis

scholarly journals Zinc finger protein X-linked promotes expansion of EpCAM+cancer stem-like cells in hepatocellular carcinoma

2017 ◽  
Vol 11 (5) ◽  
pp. 455-469 ◽  
Author(s):  
Chao Wang ◽  
Si-yuan Fu ◽  
Ming-da Wang ◽  
Wen-bo Yu ◽  
Qin-shu Cui ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Finger Protein ◽  
Protein X

scholarly journals ZNF667 Serves as a Putative Oncogene in Human Hepatocellular Carcinoma

2017 ◽  
Vol 41 (6) ◽  
pp. 2523-2533 ◽  
Author(s):  
Ke Cheng ◽  
Zhizhao Chen ◽  
Lian Liu ◽  
Yujun Zhao ◽  
Sheng Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Clinical Stage ◽  
Migration And Invasion ◽  
Bax Protein ◽  
Finger Protein ◽  
Immuno Histochemistry ◽  
Set Up

Background/Aims: Zinc finger protein 667 (ZNF667) is a member of C2H2 zinc finger protein family. For the first time, we aim to analyze the expression pattern of ZNF667 in hepatocellular carcinoma (HCC) tissues; to explore its role in HCC tumorigenesis. Methods: Immuno-histochemistry was carried out to characterize the ZNF667 expression in paraffin-embedded HCC samples. The relationship between ZNF667 expression and the clinical, pathological data of the patients were analyzed. Human normal hepatocyte cells LO2 over expressing ZNF667 (LO2-ZNF667 cells), ZNF667 depleted hepatocellular carcinoma HepG2 cells (HepG2-shZNF667 cells) were set up, their proliferation, migration and invasion abilities were analyzed. Xenograft nude mice were used to analyze the malignancy of HepG2-shZNF667 cells in vivo. Western blot was performed to analyze the expression of Bcl-2 and BAX in LO2-ZNF667 and HepG2-shZNF667 cells. Results: Increased ZNF667 was found via immuno-histochemistry in HCC. Enhanced ZNF667 expression was associated with tumor size, clinical stage and tumor differentiation. LO2-ZNF667 cells displayed increased and HepG2-shZNF667 cells decreased cell proliferation, migration and invasion. Xenograft experiments proved reduced malignancy of HepG2-shZNF667 cells in vivo. LO2-ZNF667 cells displayed increased Bcl-2 and decreased BAX protein expression. HepG2-shZNF667 cells displayed enhanced BAX and inhibited BCL-2 expression. Conclusions: ZNF667 is shown to be a new oncogene in HCC and it may serve as a new therapeutic target for HCC via enhancing BCL-2 and decreasing BAX expression.

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