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Effect of down-regulation of HE4 gene expression on biologic behavior of ovarian cancer cells / 中华病理学杂志
Chinese Journal of Pathology ; (12): 687-690, 2013.
Artículo en Chino | WPRIM | ID: wpr-288235
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of HE4 gene knockdown on the proliferation, adhesion and invasion of the ovarian cancer cells SKOV3.</p><p><b>METHODS</b>The knockdown of HE4 gene was performed by RNAi technology. The recombinant plasmids (pSUPER-HE4 shDNAs) were constructed and transfected into human ovarian cancer cells SKOV3. HE4 expression was then identified by real-time PCR and Western blot analysis. The invasion and adhesion ability of transduced cells were determined. In addition, cell proliferation and growth were analyzed by colonies formation assay.</p><p><b>RESULTS</b>Knockdown of HE4 was achieved, and further confirmed by real-time PCR and Western blot. The proliferation of HE4-down-regulated cells was not affected, but the invasion ability of the transfected cells was reduced (P < 0.05) and the adhesion ability was also reduced to 27.3%.</p><p><b>CONCLUSION</b>HE4 expression is down-regulated effectively by the constructed HE4 shDNA, and thus knockdown of HE4 inhibits the adhesion and invasion of SKOV3 cells.</p>
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Neoplasias Ováricas / Patología / Plásmidos / Proteínas Recombinantes / ARN Mensajero / Transfección / Proteínas / Regulación hacia Abajo / Regulación Neoplásica de la Expresión Génica / Adhesión Celular Límite: Femenino / Humanos Idioma: Chino Revista: Chinese Journal of Pathology Año: 2013 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Neoplasias Ováricas / Patología / Plásmidos / Proteínas Recombinantes / ARN Mensajero / Transfección / Proteínas / Regulación hacia Abajo / Regulación Neoplásica de la Expresión Génica / Adhesión Celular Límite: Femenino / Humanos Idioma: Chino Revista: Chinese Journal of Pathology Año: 2013 Tipo del documento: Artículo