Proteomic analysis of primary esophageal squamous cell carcinoma reveals downregulation of a cell adhesion protein, periplakin

PROTEOMICS ◽  
2006 ◽  
Vol 6 (3) ◽  
pp. 1011-1018 ◽  
Author(s):  
Takanori Nishimori ◽  
Takeshi Tomonaga ◽  
Kazuyuki Matsushita ◽  
Masamichi Oh-Ishi ◽  
Yoshio Kodera ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Adhesion ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Proteomic Analysis ◽  
Adhesion Protein ◽  
Cell Adhesion Protein ◽  
A Cell

iTRAQ-based quantitative proteomic analysis of esophageal squamous cell carcinoma

Tumor Biology ◽  
2015 ◽  
Vol 37 (2) ◽  
pp. 1909-1918 ◽  
Author(s):  
Feiyan Deng ◽  
Keming Zhou ◽  
Qiaoxin Li ◽  
Dong Liu ◽  
Mengyan Li ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Proteomic Analysis ◽  
Quantitative Proteomic Analysis

scholarly journals Circ0120816 acts as an oncogene of esophageal squamous cell carcinoma by inhibiting miR-1305 and releasing TXNRD1

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Xiaoyong Li ◽  
Laichun Song ◽  
Bo Wang ◽  
Chao Tao ◽  
Lei Shi ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Adhesion ◽  
Esophageal Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Luciferase Reporter ◽  
Pcr Analysis ◽  
Tissue Samples ◽  
Tumor Growth And Metastasis

Abstract Background Circular RNAs (circRNAs) have been discovered to participate in the carcinogenesis of multiple cancers. However, the role of circRNAs in esophageal squamous cell carcinoma (ESCC) progression is yet to be properly understood. This research aimed to investigate and understand the mechanism used by circRNAs to regulate ESCC progression. Methods Bioinformatics analysis was first performed to screen dysregulated circRNAs and differentially expressed genes in ESCC. The ESCC tissue samples and adjacent normal tissue samples utilized in this study were obtained from 36 ESCC patients. All the samples were subjected to qRT-PCR analysis to identify the expression of TXNRD1, circRNAs, and miR-1305. Luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay were later conducted to verify the existing relationship among circ0120816, miR-1305 and TXNRD1. CCK-8, BrdU, cell adhesion, cell cycle, western blot and caspase 3 activity assays were also employed to evaluate the regulation of these three biological molecules in ESCC carcinogenesis. To evaluate the effect of circ0120816 on ESCC tumor growth and metastasis, the xenograft mice model was constructed. Results Experimental investigations revealed that circ0120816 was the highest upregulated circRNA in ESCC tissues and that this non-coding RNA acted as a miR-1305 sponge in enhancing cell viability, cell proliferation, and cell adhesion as well as repressing cell apoptosis in ESCC cell lines. Moreover, miR-1305 was observed to exert a tumor-suppressive effect in ESCC cells by directly targeting and repressing TXNRD1. It was also noticed that TXNRD1 could regulate cyclin, cell adhesion molecule, and apoptosis-related proteins. Furthermore, silencing circ0120816 was found to repress ESCC tumor growth and metastasis in vivo. Conclusions This research confirmed that circ0120816 played an active role in promoting ESCC development by targeting miR-1305 and upregulating oncogene TXNRD1.

Discovery of stage-related proteins in esophageal squamous cell carcinoma using proteomic analysis

2007 ◽  
Vol 1 (3) ◽  
pp. 312-320 ◽  
Author(s):  
Dong-Ping Liu ◽  
Robert Z. Qi ◽  
Yan Wang ◽  
Ping-Ping Chen ◽  
H. Phillip Koeffler ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Proteomic Analysis ◽  
Related Proteins

scholarly journals O218 E-CADHERIN EXPRESSION CORRELATES WITH PROGRESSION OF ESOPHAGEAL SQUAMOUS CELL CARCINOMA

2019 ◽  
Vol 32 (Supplement_2) ◽  
Author(s):  
Hanako Koda ◽  
Kazuhiko Yamada ◽  
Masayoshi Terayama ◽  
Sumiya Ryusuke ◽  
Kyoko Nohara ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Adhesion ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Immunohistochemical Staining ◽  
Clinicopathological Features ◽  
Normal Epithelium ◽  
E Cadherin ◽  
Cell Cell

Abstract Background & Aim E-cadherin is a member of the cadherin family and plays a major role in cell–cell adhesion of normal epithelium. Decreased or lack of E-cadherin expression has been reported in breast, colon and bladder cancer, and the disruption of the E-cadherin-mediated cell–cell adhesion is considered the first crucial step of metastasis. The esophageal stratified epithelial cells have many spines that intermingle with each other through desmosomes, in which E-cadherins play an important role for cell–cell adhesion. However, the significance of E-cadherin expression in the progression of esophageal squamous cell carcinoma (ESCC) still remains to be clarified. In the present study, we investigated the relation between E-cadherin expression in tumors and the clinicopathological features of ESCC. Method E-cadherin expression was evaluated in ESCC specimens of 61 patients who underwent surgery from April 2008 to December 2015 at the National Center for Global Health and Medicine by immunohistochemical staining. Distribution of E-cadherin in cancerous tissues was classified as Preserved (expression in cell membrane alone) or Disturbed (expression in cytoplasm or decreased/lack of expression of E-cadherin). Significance of the distribution pattern was analyzed by comparison to clinicopathological features. Results Thirty-seven of 61 (61%) cases revealed Preserved expression pattern while Disturbed distribution was observed in 24 of 61 (39%) cases. Compared to Preserved pattern, Disturbed expression of E-cadherin in tumors was significantly associated with advanced TNM stages (P=0.0462). Conclusion E-cadherin was expressed in most cases of ESCC; however, its distribution was not restricted in membrane but in the cytoplasm of tumors. Disturbed expression of E-cadherin in tumors correlated with advanced stage of ESCC, suggesting that the disruption of the E-cadherin-mediated cell–cell adhesion may play an important role in the progression of ESCC.

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