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[Inhibitory effect of exogenous insulin-like growth factor binding protein 7 on proliferation of human breast cancer cell line MDA-MB-453 and its mechanism].
Yuan, Lei; Fan, Wen-Juan; Yang, Xu-Guang; Rao, Shu-Mei; Song, Jin-Ling; Song, Guo-Hua.
Afiliación
  • Yuan L; Laboratory of Molecular Biology, Luohe Medical College, Luohe 462002, China. lhyzsgh@163.com.
Sheng Li Xue Bao ; 65(5): 519-24, 2013 Oct 25.
Article en Zh | MEDLINE | ID: mdl-24129733
ABSTRACT
The present study was to investigate the effects of exogenous insulin-like growth factor binding protein 7 (IGFBP7) on the proliferation of human breast cancer cell line MDA-MB-453 and its possible mechanism. By means of MTT method in vitro, the results showed exogenous IGFBP7 inhibited the growth of MDA-MB-453 cells (IC50 of IGFBP7 = 8.49 µg/mL) in time- and concentration-dependent manner. SB203580, p38(MAPK) inhibitor, blocked the anti-proliferative effect of exogenous IGFBP7. The flow cytometry assay showed that exogenous IGFBP7 remarkably induced G0/G1 arrest in MDA-MB-453 cells. The Western blot showed that exogenous IGFBP7 promoted phosphorylation of p38(MAPK), up-regulated expression of p21(CIP1/WAF1), and inhibited phosphorylation of Rb. SB203580 restrained exogenous IGFBP7-induced regulation of p21(CIP1/WAF1) and p-Rb in MDA-MB-453 cells. In conclusion, the present study suggests that exogenous IGFBP7 could activate the p38(MAPK) signaling pathway, upregulate p21(CIP1/WAF1) expression, inhibit phosphorylation of Rb, and finally induce G0/G1 arrest in MDA-MB-453 cells.
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Bases de datos: MEDLINE Asunto principal: Neoplasias de la Mama / Proteínas de Unión a Factor de Crecimiento Similar a la Insulina / Proliferación Celular Límite: Female / Humans Idioma: Zh Revista: Sheng Li Xue Bao Año: 2013 Tipo del documento: Article País de afiliación: China
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Bases de datos: MEDLINE Asunto principal: Neoplasias de la Mama / Proteínas de Unión a Factor de Crecimiento Similar a la Insulina / Proliferación Celular Límite: Female / Humans Idioma: Zh Revista: Sheng Li Xue Bao Año: 2013 Tipo del documento: Article País de afiliación: China