scholarly journals Inhibiting Forkhead box K1 induces autophagy to reverse epithelial-mesenchymal transition and metastasis in gastric cancer by regulating Myc-associated zinc finger protein in an acidic microenvironment

Aging ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 6129-6150 ◽  
Author(s):  
Yixuan Wang ◽  
Libin Sun ◽  
Wensheng Qiu ◽  
Weiwei Qi ◽  
Yaoyue Qi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Acidic Microenvironment ◽  
Forkhead Box ◽  
Finger Protein

scholarly journals The Zinc-Finger Protein Slug Causes Desmosome Dissociation, an Initial and Necessary Step for Growth Factor–induced Epithelial–Mesenchymal Transition

1997 ◽  
Vol 137 (6) ◽  
pp. 1403-1419 ◽  
Author(s):  
Pierre Savagner ◽  
Kenneth M. Yamada ◽  
Jean Paul Thiery
Keyword(s):  
Growth Factor ◽  
Zinc Finger ◽  
Cell Separation ◽  
Zinc Finger Protein ◽  
Epithelial Mesenchymal Transition ◽  
Cell Spreading ◽  
Cell Contact ◽  
Mesenchymal Transition ◽  
Finger Protein ◽  
Cell Cell

Epithelial–mesenchymal transition (EMT) is an essential morphogenetic process during embryonic development. It can be induced in vitro by hepatocyte growth factor/scatter factor (HGF/SF), or by FGF-1 in our NBT-II cell model for EMT. We tested for a central role in EMT of a zinc-finger protein called Slug. Slug mRNA and protein levels were increased transiently in FGF-1–treated NBT-II cells. Transient or stable transfection of Slug cDNA in NBT-II cells resulted in a striking disappearance of the desmosomal markers desmoplakin and desmoglein from cell–cell contact areas, mimicking the initial steps of FGF-1 or HGF/SF- induced EMT. Stable transfectant cells expressed Slug protein and were less epithelial, with increased cell spreading and cell–cell separation in subconfluent cultures. Interestingly, NBT-II cells transfected with antisense Slug cDNA were able to resist EMT induction by FGF-1 or even HGF/SF. This antisense effect was suppressed by retransfection with Slug sense cDNA. Our results indicate that Slug induces the first phase of growth factor–induced EMT, including desmosome dissociation, cell spreading, and initiation of cell separation. Moreover, the antisense inhibition experiments suggest that Slug is also necessary for EMT.

Zinc-finger protein 545 is a novel tumour suppressor that acts by inhibiting ribosomal RNA transcription in gastric cancer

Gut ◽  
2012 ◽  
Vol 62 (6) ◽  
pp. 833-841 ◽  
Author(s):  
Shiyan Wang ◽  
Yingduan Cheng ◽  
Wan Du ◽  
Leina Lu ◽  
Liang Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Zinc Finger ◽  
Ribosomal Rna ◽  
Zinc Finger Protein ◽  
Tumour Suppressor ◽  
Rna Transcription ◽  
Finger Protein

Zinc-finger protein 331, a novel putative tumor suppressor, suppresses growth and invasiveness of gastric cancer

Oncogene ◽  
2012 ◽  
Vol 32 (3) ◽  
pp. 307-317 ◽  
Author(s):  
J Yu ◽  
Q Y Liang ◽  
J Wang ◽  
Y Cheng ◽  
S Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Finger Protein ◽  
Putative Tumor Suppressor

scholarly journals Poor survival is associated with the methylated degree of zinc-finger protein 545 (ZNF545) DNA promoter in gastric cancer

Oncotarget ◽  
2015 ◽  
Vol 6 (6) ◽  
pp. 4482-4495 ◽  
Author(s):  
Jingyu Deng ◽  
Han Liang ◽  
Guoguang Ying ◽  
Qiuping Dong ◽  
Rupeng Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Poor Survival ◽  
Finger Protein

Zinc-Finger Protein 471 Functions as a Tumor Suppressor in Gastric Cancer through Transcriptionally Repressing TFAP2A and PLS3

2017 ◽  
Vol 152 (5) ◽  
pp. S801-S802
Author(s):  
Lei Cao ◽  
Shiyan Wang ◽  
Yanquan Zhang ◽  
Ka Chun Wong ◽  
Daniel Nakatsu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Suppressor ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Finger Protein

scholarly journals Y-Box Binding Protein-1 Promotes Epithelial-Mesenchymal Transition in Sorafenib-Resistant Hepatocellular Carcinoma Cells

2020 ◽  
Vol 22 (1) ◽  
pp. 224
Author(s):  
Li-Zhu Liao ◽  
Chih-Ta Chen ◽  
Nien-Chen Li ◽  
Liang-Chun Lin ◽  
Bo-Shih Huang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Epithelial Mesenchymal Transition ◽  
Binding Protein ◽  
The Cancer Genome Atlas ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Mesenchymal Transition

Hepatocellular carcinoma is one of the most common cancer types worldwide. In cases of advanced-stage disease, sorafenib is considered the treatment of choice. However, resistance to sorafenib remains a major obstacle for effective clinical application. Based on integrated phosphoproteomic and The Cancer Genome Atlas (TCGA) data, we identified a transcription factor, Y-box binding protein-1 (YB-1), with elevated phosphorylation of Ser102 in sorafenib-resistant HuH-7R cells. Phosphoinositide-3-kinase (PI3K) and protein kinase B (AKT) were activated by sorafenib, which, in turn, increased the phosphorylation level of YB-1. In functional analyses, knockdown of YB-1 led to decreased cell migration and invasion in vitro. At the molecular level, inhibition of YB-1 induced suppression of zinc-finger protein SNAI1 (Snail), twist-related protein 1 (Twist1), zinc-finger E-box-binding homeobox 1 (Zeb1), matrix metalloproteinase-2 (MMP-2) and vimentin levels, implying a role of YB-1 in the epithelial-mesenchymal transition (EMT) process in HuH-7R cells. Additionally, YB-1 contributes to morphological alterations resulting from F-actin rearrangement through Cdc42 activation. Mutation analyses revealed that phosphorylation at S102 affects the migratory and invasive potential of HuH-7R cells. Our collective findings suggest that sorafenib promotes YB-1 phosphorylation through effect from the EGFR/PI3K/AKT pathway, leading to significant enhancement of hepatocellular carcinoma (HCC) cell metastasis. Elucidation of the specific mechanisms of action of YB-1 may aid in the development of effective strategies to suppress metastasis and overcome resistance.

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