scholarly journals Mammary serine protease inhibitor inhibits epithelial growth factor-induced epithelial-mesenchymal transition of esophageal carcinoma cells

Cancer ◽  
2008 ◽  
Vol 115 (1) ◽  
pp. 36-48 ◽  
Author(s):  
Zhen Cai ◽  
Yuan Zhou ◽  
Ting Lei ◽  
Jen-Fu Chiu ◽  
Qing-Yu He
Keyword(s):  
Growth Factor ◽  
Protease Inhibitor ◽  
Esophageal Carcinoma ◽  
Serine Protease ◽  
Epithelial Mesenchymal Transition ◽  
Serine Protease Inhibitor ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Epithelial Growth Factor ◽  
Epithelial Growth

scholarly journals Tazarotene-Induced Gene 1 (TIG1) Interacts with Serine Protease Inhibitor Kazal-Type 2 (SPINK2) to Inhibit Cellular Invasion of Testicular Carcinoma Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Rong-Yaun Shyu ◽  
Chun-Hua Wang ◽  
Chang-Chieh Wu ◽  
Lu-Kai Wang ◽  
Mao-Liang Chen ◽  
...  
Keyword(s):  
Protease Inhibitor ◽  
Testicular Cancer ◽  
Serine Protease ◽  
Epithelial Mesenchymal Transition ◽  
Serine Protease Inhibitor ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Testicular Carcinoma ◽  
Cancer Tissues

Tazarotene-induced gene 1 (TIG1) encodes a protein that is a retinoid-regulated tumor suppressor. TIG1 is expressed in most normal tissues, and downregulation of TIG1 expression in multiple cancers is caused by promoter hypermethylation. Kazal-type serine protease inhibitor-2 (SPINK2) is a serine protease inhibitor, and the SPINK protein family has been shown to inhibit the expression of urokinase-type plasminogen activator (uPA). In addition, increased levels of uPA and the uPA receptor were observed in testicular cancer tissues. This study demonstrated that TIG1 interacts with SPINK2 in NT2/D1 testicular carcinoma cells. TIG1 and SPINK2 were highly expressed in normal testis tissues, while low expression levels of TIG1 and SPINK2 were found in testicular cancer tissues. TIG1 inhibited cell invasion, migration, and epithelial–mesenchymal transition (EMT) of NT2/D1 cells. SPINK2 enhanced TIG1-regulated uPA activity and EMT suppression, while silencing SPINK2 alleviated TIG1-mediated EMT regulation, cell migration, and invasion. Therefore, the results suggest that the interaction between TIG1 and SPINK2 plays an important role in the inhibition of testicular cancer cell EMT, and suppression is mediated through downregulation of the uPA/uPAR signaling pathway.

scholarly journals Significance of epithelial growth factor in the epithelial-mesenchymal transition of human gallbladder cancer cells

2012 ◽  
Vol 103 (6) ◽  
pp. 1165-1171 ◽  
Author(s):  
Takamitsu Sasaki ◽  
Hiroki Kuniyasu ◽  
Yi Luo ◽  
Daisuke Kato ◽  
Satoshi Shinya ◽  
...  
Keyword(s):  
Growth Factor ◽  
Gallbladder Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Human Gallbladder ◽  
Mesenchymal Transition ◽  
Epithelial Growth Factor ◽  
Epithelial Growth

scholarly journals Long non-coding (lnc)RNA profiling and the role of a key regulator lnc-PNRC2-1 in the transforming growth factor-β1-induced epithelial–mesenchymal transition of CNE1 nasopharyngeal carcinoma cells

2021 ◽  
Vol 49 (3) ◽  
pp. 030006052199651
Author(s):  
Jie Yang ◽  
Enzi Feng ◽  
Yanxin Ren ◽  
Shun Qiu ◽  
Liufang Zhao ◽  
...  
Keyword(s):  
Growth Factor ◽  
Nasopharyngeal Carcinoma ◽  
Rna Sequencing ◽  
Western Blotting ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Emt Markers ◽  
Tgf Β1

Objectives To identify key long non-coding (lnc)RNAs responsible for the epithelial–mesenchymal transition (EMT) of CNE1 nasopharyngeal carcinoma cells and to investigate possible regulatory mechanisms in EMT. Methods CNE1 cells were divided into transforming growth factor (TGF)-β1-induced EMT and control groups. The mRNA and protein expression of EMT markers was determined by real-time quantitative PCR and western blotting. Differentially expressed genes (DEGs) between the two groups were identified by RNA sequencing analysis, and DEG functions were analyzed by gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses. EMT marker expression was re-evaluated by western blotting after knockdown of a selected lncRNA. Results TGF-β1-induced EMT was characterized by decreased E-cadherin and increased vimentin, N-cadherin, and Twist expression at both mRNA and protein levels. Sixty lncRNA genes were clustered in a heatmap, and mRNA expression of 14 dysregulated lncRNAs was consistent with RNA sequencing. Knockdown of lnc-PNRC2-1 increased expression of its antisense gene MYOM3 and reduced expression of EMT markers, resembling treatment with the TGF-β1 receptor inhibitor LY2109761. Conclusion Various lncRNAs participated indirectly in the TGF-β1-induced EMT of CNE1 cells. Lnc-PNRC2-1 may be a key regulator of this and is a potential target to alleviate CNE1 cell EMT.

scholarly journals Cripto-1 Promotes the Epithelial-Mesenchymal Transition in Esophageal Squamous Cell Carcinoma Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Chun Huang ◽  
Wangsheng Chen ◽  
Xiaowen Wang ◽  
Jinqiu Zhao ◽  
Qian Li ◽  
...  
Keyword(s):  
Esophageal Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Public Health Problem ◽  
Carcinoma Cells ◽  
Malignant Neoplasms ◽  
Major Public Health Problem ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
Tumorigenesis And Progression ◽  
Made In

Esophageal carcinoma is a major public health problem worldwide and one of the most aggressively malignant neoplasms. Although considerable diagnostic and therapeutic progress has been made in recent years, the prognosis of EC patients still remains dismal due to high rates of recurrence/metastasis and invasion. Previous studies have demonstrated that Epithelial mesenchymal transition (EMT) is proposed as a critical mechanism for the acquisition of malignant phenotypes by epithelial cells. Several lines of evidence have shown that Cripto-1 plays an important oncogenic role during tumorigenesis by promoting EMT. The aim of our study was to evaluate the significance of Cripto-1 which plays a role in EMT and its metastasis in esophageal carcinoma. Data of this study suggest that Cripto-1 overexpression is connected with the tumorigenesis and progression of esophageal carcinoma; shRNA might be feasible for the inhibition of the invasion and metastasis of esophageal carcinoma.

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