Correlation between the overexpression of epidermal growth factor receptor and mesenchymal makers in endometrial carcinoma / 부인종양
Journal of Gynecologic Oncology
;
: 36-42, 2014.
Artículo
en Inglés
| WPRIM
| ID: wpr-202950
ABSTRACT
OBJECTIVE:
The objective of this study was to evaluate the effect of overexpression of epidermal growth factor receptor (EGFR) on the expression of epithelial cell markers (E-cadherin and alpha-catenin) and mesenchymal cell markers (N-cadherin and vimentin) in endometrial carcinoma.METHODS:
The expression of all 4 markers was evaluated in EGFR overexpressing Ishikawa cells, control Ishikawa cells, and KLE cells using reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. The expression of these 4 markers was also determined in cancerous tissues of patients with endometrial carcinoma using immunohistochemical staining.RESULTS:
Ishikawa cells transfected with EGFR showed decreased expression of E-cadherin and alpha-catenin and increased expression of N-cadherin and vimentin compared with control Ishikawa cells (p<0.01 for all). The expression of N-cadherin and vimentin was higher and the expression of E-cadherin and alpha-catenin was lower in stage II-III than stage I and in grade II-III than grade I endometrial carcinoma tissue (p<0.01 for all).CONCLUSION:
Decreased expression of epithelial markers (E-cadherin and alpha-catenin) and increased expression of mesenchymal markers (N-cadherin and vimentin) were observed in human endometrial carcinoma tissue. These findings correlate with high EGFR expression in cultured endometrial carcinoma cells.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Vimentina
/
Cadherinas
/
Western Blotting
/
Reacción en Cadena de la Polimerasa
/
Neoplasias Endometriales
/
Transcripción Reversa
/
Factor de Crecimiento Epidérmico
/
Células Epiteliales
/
Alfa Catenina
/
Transición Epitelial-Mesenquimal
Límite:
Femenino
/
Humanos
Idioma:
Inglés
Revista:
Journal of Gynecologic Oncology
Año:
2014
Tipo del documento:
Artículo
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