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Chinese Journal of Oncology ; (12): 495-499, 2007.
Artigo em Chinês | WPRIM | ID: wpr-298566

RESUMO

<p><b>OBJECTIVE</b>To study the effects and mechanism of apigenin on the expression of vascular endothelial growth factor (VEGF) in human breast cancer MDA-MB-231 cells.</p><p><b>METHODS</b>MDA-MB-231 cells were used as the study object. MTT assay was used to detect the effect of apigenin on the cell viability. ELISA was used to determine the protein level of VEGF. RT-PCR was used to detect VEGF at mRNA level. A double luciferase system was used to measure the transcription activity of VEGF. pCEP4-HIF-1alpha was transferred to explore the reversing effect of HIF-1alpha on the inhibitory effect of apigenin on the transcription activity of VEGF. Western blotting was used to detect the time-dependent and dose-dependent effect of apigenin on HIF-lalpha, p-AKT, p-ERK, and p53 expression at protein level.</p><p><b>RESULTS</b>Apigenin had no visible inhibitory effect on cell viability. Apigenin reduced the secretion of VEGF, mRNA levels of VEGF and transcription activity of VEGF. Furthermore, the inhibitory effect of apigenin on the transcription activity of VEGF could be reversed by transferring pCEP4-HIF-1alpha into the cells. Additionally, apigenin inhibited the expression of HIF-1alpha and p-AKT, induced the expression of p53, but had no effect on the expression of p-ERK1/2.</p><p><b>CONCLUSION</b>Apigenin can inhibit VEGF expression in breast cancer cells, and this effect may be achieved through decreasing the expression of HIF-1alpha.</p>


Assuntos
Feminino , Humanos , Antineoplásicos Fitogênicos , Farmacologia , Apigenina , Farmacologia , Neoplasias da Mama , Metabolismo , Patologia , Linhagem Celular Tumoral , Regulação Neoplásica da Expressão Gênica , Subunidade alfa do Fator 1 Induzível por Hipóxia , Genética , Metabolismo , Proteína Quinase 3 Ativada por Mitógeno , Metabolismo , Fosforilação , Proteínas Proto-Oncogênicas c-akt , Metabolismo , RNA Mensageiro , Metabolismo , Ativação Transcricional , Proteína Supressora de Tumor p53 , Metabolismo , Fator A de Crescimento do Endotélio Vascular , Genética , Metabolismo
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