scholarly journals Induction of α2-antiplasmin inhibits E-cadherin processing mediated by the plasminogen activator/plasmin system, leading to suppression of progression of oral squamous cell carcinoma via upregulation of cell-cell adhesion

2007 ◽  
Author(s):  
Yasutaka Hayashido ◽  
Tomoaki Hamana ◽  
Yasutaka Ishida ◽  
Tomoaki Shintani ◽  
Koh-ichi Koizumi ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Adhesion ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Plasminogen Activator ◽  
Squamous Cell ◽  
E Cadherin ◽  
Cell Cell

Expression of the cell-cell adhesion molecule E-cadherin in squamous cell carcinoma of the head and neck

2007 ◽  
Vol 18 (3) ◽  
pp. 196-201 ◽  
Author(s):  
GAYLE L. BOWIE ◽  
A.W. CASLIN ◽  
N.J. ROLAND ◽  
J.K.K. MA. FIELD ◽  
A.S. JONES ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Adhesion ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
E Cadherin ◽  
Cell Cell

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.

scholarly journals EKSPRESI p53 DAN E-CADHERIN SEBAGAI PREDIKTOR PROGNOSIS PADA KARSINOMA SEL SKUAMOSA RONGGA MULUT DI RSUP DR. KARIADI SEMARANG

2019 ◽  
Vol 5 (1) ◽  
pp. 7-17
Author(s):  
Clara Pangaribuan
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
E Cadherin

p53 AND E-CADHERIN EXPRESSION AS  PREDICTORS OF PROGNOSTIC IN ORAL SQUAMOUS CELL CARCINOMA AT KARIADI HOSPITAL SEMARANG

scholarly journals Patients with advanced oral squamous cell carcinoma have high levels of soluble E-cadherin in the saliva

2017 ◽  
pp. 0-0
Author(s):  
S Lopez-Verdin ◽  
JJ Soto-Avila ◽  
AL Zamora-Perez ◽  
BP Lazalde-Ramos ◽  
ML Martinez-Fierro ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
E Cadherin

The transcription factor Snail enhanced the degradation of E-cadherin and desmoglein 2 in oral squamous cell carcinoma cells

2013 ◽  
Vol 430 (3) ◽  
pp. 889-894 ◽  
Author(s):  
Kenichi Kume ◽  
Misako Haraguchi ◽  
Hiroshi Hijioka ◽  
Takayuki Ishida ◽  
Akihiko Miyawaki ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Transcription Factor ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Carcinoma Cells ◽  
E Cadherin

Podoplanin and E-cadherin Expression in Preoperative Incisional Biopsies of Oral Squamous Cell Carcinoma Is Related to Lymph Node Metastases

2013 ◽  
Vol 21 (2) ◽  
pp. 133-141 ◽  
Author(s):  
Maria P. Foschini ◽  
Elisa Leonardi ◽  
Leonardo Henry Eusebi ◽  
Anna Farnedi ◽  
Tito Poli ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Lymph Node ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Lymph Node Metastases ◽  
Node Metastases ◽  
E Cadherin

scholarly journals NF-κB-mediated lncRNA AC007271.3 promotes carcinogenesis of oral squamous cell carcinoma by regulating miR-125b-2-3p/Slug

2020 ◽  
Vol 11 (12) ◽  
Author(s):  
Ze-nan Zheng ◽  
Guang-zhao Huang ◽  
Qing-qing Wu ◽  
Heng-yu Ye ◽  
Wei-sen Zeng ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Molecular Mechanisms ◽  
Nuclear Factor Κb ◽  
Underlying Mechanisms ◽  
E Cadherin

AbstractOral squamous cell carcinoma (OSCC) is the most common oral cancer. The molecular mechanisms of this disease are not fully understood. Our previous studies confirmed that dysregulated function of long non-coding RNA (lncRNA) AC007271.3 was associated with a poor prognosis and overexpression of AC007271.3 promoted cell proliferation, migration, invasion, and inhibited cell apoptosis in vitro, and promoted tumor growth in vivo. However, the underlying mechanisms of AC007271.3 dysregulation remained obscure. In this study, our investigation showed that AC007271.3 functioned as competing endogenous RNA by binding to miR-125b-2-3p and by destabilizing primary miR-125b-2, resulted in the upregulating expression of Slug, which is a direct target of miR-125b-2-3p. Slug also inhibited the expression of E-cadherin but N-cadherin, vimentin, and β-catenin had no obvious change. The expression of AC007271.3 was promoted by the canonical nuclear factor-κB (NF-κB) pathway. Taken together, these results suggested that the classical NF-κB pathway-activated AC007271.3 regulates EMT by miR-125b-2-3p/Slug/E-cadherin axis to promote the development of OSCC, implicating it as a novel potential target for therapeutic intervention in this disease.

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