scholarly journals High Expression of Peroxiredoxin 1 Is Associated with Epithelial-Mesenchymal Transition Marker and Poor Prognosis in Gastric Cancer

2018 ◽  
Vol 24 ◽  
pp. 2259-2270 ◽  
Author(s):  
Wei Yu ◽  
Jing Wu ◽  
Zhong-liang Ning ◽  
Qiao-yu Liu ◽  
Rui-liang Quan
Keyword(s):  
Gastric Cancer ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
High Expression ◽  
Mesenchymal Transition ◽  
Peroxiredoxin 1

scholarly journals Plastin3 is associated with epithelial‑mesenchymal transition and poor prognosis in gastric cancer

2018 ◽  
Author(s):  
Junji Kurashige ◽  
Takehiro Yokobori ◽  
Kosuke Mima ◽  
Genta Sawada ◽  
Yusuke Takahashi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals CD146 Expression Correlates with Epithelial-Mesenchymal Transition Markers and a Poor Prognosis in Gastric Cancer

2012 ◽  
Vol 13 (5) ◽  
pp. 6399-6406 ◽  
Author(s):  
Wen-Fang Liu ◽  
Shu-Rong Ji ◽  
Jian-Jun Sun ◽  
Yi Zhang ◽  
Zhong-Yan Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Cd146 Expression

scholarly journals The High Expression of CD276/HAVCR2 and CD163 is an Adverse Immune Subtype of Glioblastoma and is Closely Related to Epithelial-Mesenchymal Transition

2020 ◽  
Author(s):  
Xiaohong Hou ◽  
Guiyin Zhou ◽  
Yinchun Fan ◽  
Qiang Zhang ◽  
Chengming Xiang ◽  
...  
Keyword(s):  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Malignant Tumors ◽  
Checkpoint Inhibitors ◽  
Enrichment Analysis ◽  
R Package ◽  
High Expression ◽  
Sequencing Data ◽  
Mesenchymal Transition ◽  
Patient Prognosis

Abstract Background Glioblastoma (GBM) is one of the most malignant tumors that can afflict the central nervous system. Previous studies have observed that there are individual differences in the treatment response of immune checkpoint inhibitors in glioblastoma. This study’s aim is to ascertain the factors that may affect the efficacy of immunosuppressant therapy. Methods The clinical data of this study were obtained from a public database. Then, the data was analyzed and processed by R software and corresponding R package. To verify the results of the analysis, information was gathered from 89 GBM patients in our hospital and thereafter the corresponding paraffin sections were stained and quantitatively analyzed by immunohistochemistry. Results From the analysis, it was observed that both CD276 and HAVCR2 were significantly overexpressed in GBM and could be associated with patient prognosis. The analysis of single cell RNA sequencing data and GBM data analysis found an immune subtype with poor prognosis. Further analysis found that the high expression of CD276, HAVCR2 and CD163 was closely related to epithelial-mesenchymal transition (EMT) and could affect the patient prognosis of PD-L1 high expression. GSVA enrichment analysis showed that CD276, HAVCR2 and CD163 might induce EMT by JAK-STAT3 signaling pathway, and RUNX1 and IKZF1 might be transcription factors that regulate CD276/HAVCR2 high expression. Conclusions We found an immune subtype with poor prognosis of GBM, the high expression of CD276, HAVCR2 and CD163 with EMT are closely related and may be one of the factors affecting the efficacy of Anti-PD-L1.

scholarly journals CXCR6 predicts poor prognosis in gastric cancer and promotes tumor metastasis through epithelial-mesenchymal transition

2017 ◽  
Vol 37 (6) ◽  
pp. 3279-3286 ◽  
Author(s):  
Jie-Jie Jin ◽  
Fa-Xiang Dai ◽  
Zi-Wen Long ◽  
Hong Cai ◽  
Xiao-Wen Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Poor Prognosis ◽  
Tumor Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition

Weighted correlation network analysis identifies FN1, COL1A1 and SERPINE1 associated with the progression and prognosis of gastric cancer

2021 ◽  
pp. 1-17
Author(s):  
Qiaoyun Zhao ◽  
Jun Xie ◽  
Jinliang Xie ◽  
Rulin Zhao ◽  
Conghua Song ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Correlation Network ◽  
Receptor Interaction ◽  
Hub Genes ◽  
Mesenchymal Transition ◽  
Weighted Correlation

BACKGROUND: Gastric cancer (GC) is one of the most deadliest tumours worldwide, and its prognosis remains poor. OBJECTIVE: This study aims to identify and validate hub genes associated with the progression and prognosis of GC by constructing a weighted correlation network. METHODS: The gene co-expression network was constructed by the WGCNA package based on GC samples and clinical data from the TCGA database. The module of interest that was highly related to clinical traits, including stage, grade and overall survival (OS), was identified. GO and KEGG pathway enrichment analyses were performed using the clusterprofiler package in R. Cytoscape software was used to identify the 10 hub genes. Differential expression and survival analyses were performed on GEPIA web resources and verified by four GEO datasets and our clinical gastric specimens. The receiver operating characteristic (ROC) curves of hub genes were plotted using the pROC package in R. The potential pathogenic mechanisms of hub genes were analysed using gene set enrichment analysis (GSEA) software. RESULTS: A total of ten modules were detected, and the magenta module was identified as highly related to OS, stage and grade. Enrichment analysis of magenta module indicated that ECM-receptor interaction, focal adhesion, PI3K-Akt pathway, proteoglycans in cancer were significantly enriched. The PPI network identified ten hub genes, namely COL1A1, COL1A2, FN1, POSTN, THBS2, COL11A1, SPP1, MMP13, COMP, and SERPINE1. Three hub genes (FN1, COL1A1 and SERPINE1) were finally identified to be associated with carcinogenicity and poor prognosis of GC, and all were independent risk factors for GC. The area under the curve (AUC) values of FN1, COL1A1 and SERPINE1 for the prediction of GC were 0.702, 0.917 and 0.812, respectively. GSEA showed that three hub genes share 15 common upregulated biological pathways, including hypoxia, epithelial mesenchymal transition, angiogenesis, and apoptosis. CONCLUSION: We identified FN1, COL1A1 and SERPINE1 as being associated with the progression and poor prognosis of GC.

scholarly journals Entrectinib Induces Apoptosis and Inhibits the Epithelial–Mesenchymal Transition in Gastric Cancer with NTRK Overexpression

2021 ◽  
Vol 23 (1) ◽  
pp. 395
Author(s):  
Sung-Hwa Sohn ◽  
Hee Jung Sul ◽  
Bum Jun Kim ◽  
Hyeong Su Kim ◽  
Dae Young Zang
Keyword(s):  
Gastric Cancer ◽  
Epithelial Mesenchymal Transition ◽  
High Expression ◽  
Mechanistic Study ◽  
Sequencing Analysis ◽  
Receptor Kinase ◽  
Ags Cells ◽  
Mesenchymal Transition ◽  
Expression Levels ◽  
Gastric Cancer Patients

Tropomyosin receptor kinase (TRK) and receptor tyrosine kinase (RTK class VII) expression are important in many human diseases, especially cancers, including colorectal, lung, and gastric cancer. Using RNA sequencing analysis, we evaluated the mRNA expression and mutation profiles of gastric cancer patients with neurotropic tropomyosin receptor kinase (NTRK) 1-3 overexpression (defined as a ≥2.0-fold change). Furthermore, we screened eight TRK inhibitors in NCI-N87, SNU16, MKN28, MKN7, and AGS cells. Among these inhibitors, entrectinib showed the highest inhibitory activity; therefore, this drug was selected for analysis of its therapeutic mechanisms in gastric cancer. Entrectinib treatment induced apoptosis in NTRK1-3-expressing and VEGFR2-expressing NCI-N87 and AGS cells, but it had no effect on NTRK1-3-, VEGFR2-, TGFBR1-, and CD274-expressing MKN7 cells. SNU16 and MKN28 cells with low NTRK1-3 expression were not affected by entrectinib. Therefore, a mechanistic study was conducted in NCI-N87 (high expression of NTRK1-3 but mutation of NTRK3), AGS (high expression of NTRK1-3) and MKN28 (low expression of NTRK1-3) gastric cancer cell lines. Entrectinib treatment significantly reduced expression levels of phosphorylated NFκB, AKT, ERK, and β-catenin in NCI-N87 and AGS cells, whereas it upregulated the expression levels of ECAD in NCI-N87 cells. Together, these results suggest that entrectinib has anti-cancer activity not only in GC cells overexpressing pan NTRK but also in VEGFR2 GC cells via the inhibition of the pan NTRK and VEGFR signaling pathways.

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