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Prostaglandin E2 and Interleukin-1beta Reduce E-cadherin Expression by Enhancing Snail Expression in Gastric Cancer Cells
Journal of Korean Medical Science ; : 987-992, 2012.
Artículo en Inglés | WPRIM | ID: wpr-154194
ABSTRACT
Inflammation is closely related to the progression of cancer as well as tumorigenesis. Here, we investigated the effect of prostaglandin E2 (PGE2) and interleukin-1beta (IL-1beta) on E-cadherin expression in SNU719 gastric cancer cells. E-cadherin expression decreased as the dose or exposure time of PGE2 and IL-1beta increased, whereas Snail expression increased with dose or time of PGE2 and IL-1beta. E-cadherin expression reduced by PGE2 treatment increased after the transfection of Snail siRNA. Neutralization of IL-1beta using anti-IL-1beta antibody blocked the expression pattern of E-cadherin and Snail occurred by IL-1beta treatment. However, there was no synergic effect of IL-1beta and PGE2 on the expression pattern of E-cadherin and Snail. In conclusion, inflammatory mediators reduced E-cadherin expression by enhancing Snail expression in gastric cancer cells. Inflammation-induced transcriptional regulation of E-cadherin in gastric cancer has implications for targeted chemoprevention and therapy.
Asunto(s)

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Neoplasias Gástricas / Factores de Transcripción / Dinoprostona / Cadherinas / Regulación de la Expresión Génica / ARN Interferente Pequeño / Interferencia de ARN / Línea Celular Tumoral / Interleucina-1beta / Anticuerpos Límite: Humanos Idioma: Inglés Revista: Journal of Korean Medical Science Año: 2012 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Neoplasias Gástricas / Factores de Transcripción / Dinoprostona / Cadherinas / Regulación de la Expresión Génica / ARN Interferente Pequeño / Interferencia de ARN / Línea Celular Tumoral / Interleucina-1beta / Anticuerpos Límite: Humanos Idioma: Inglés Revista: Journal of Korean Medical Science Año: 2012 Tipo del documento: Artículo