The expression of EGFR by immunohistochemical staining to predict the response of nimotuzumab in esophageal squamous cell carcinoma.

Abstract Transient receptor potential vanilloid 2 (TRPV2) was recently shown to be involved in migrant potentials. Previous studies reported that TRPV2 was involved in cancer progression, migration, and invasion. The present study aimed to investigate its role in esophageal squamous cell carcinoma (ESCC). Methods In human ESCC cell lines, we investigated the role of TPRV2 in ESCC using a cancer function assay with the knockdown of TRPV2 by siRNA, microarray, pathway, and gene ontology analyses. The significance of TRPV2 expression in 62 ESCC samples was then evaluated by immunohistochemical staining. Results TRPV2 was overexpressed in TE15 and KYSE170 cells. TRPV2 depletion suppressed cell proliferation, cell cycle progression, and invasion/migration, and induced apoptosis. A pathway analysis of microarray data revealed that TRPV2 depletion down-regulated WNT/β-catenin signaling-related genes and basal cell carcinoma signaling-related genes. The suppression of cancer functions, such as proliferation, invasion, and angiogenesis, by TRPV2 depletion was predicted in the ontology analysis. Immunohistochemical staining revealed a relationship between strong TRPV2 expression and a poor prognosis in ESCC patients. Conclusion The present results suggest that TRPV2 regulates tumor progression by affecting WNT/β-catenin or basal cell carcinoma signaling, and that its strong expression is associated with a worse prognosis in ESCC patients. These results provide an insight into the role of TRPV2 as a therapeutic target or biomarker for ESCC.

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The relation of EGFR expression by immunohistochemical staining and clinical response of combination treatment of nimotuzumab and chemotherapy in esophageal squamous cell carcinoma

Clinical & Translational Oncology ◽

10.1007/s12094-015-1406-8 ◽

2015 ◽

Vol 18 (6) ◽

pp. 592-598 ◽

Cited By ~ 6

Author(s):

J. Jia ◽

Y. Cui ◽

M. Lu ◽

X. Wang ◽

Jie Li ◽

...

Keyword(s):

Squamous Cell Carcinoma ◽

Esophageal Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Clinical Response ◽

Squamous Cell ◽

Combination Treatment ◽

Immunohistochemical Staining ◽

Egfr Expression

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

Diseases of the Esophagus ◽

10.1093/dote/doz092.218 ◽

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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