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Research on inhibition mechanism of chlorogenic acid for colorectal cancer cell line HCT116 / 中草药
Chinese Traditional and Herbal Drugs ; (24): 4952-4957, 2017.
Artigo em Chinês | WPRIM | ID: wpr-852357
ABSTRACT
Objective To discuss the inhibition mechanism of chlorogenic acid for colorectal cancer cell line HCT116. Methods Colorectal cancer cell line HCT116 were treated with chlorogenic acid, and the untreated group was blank control. Then, the gene expression chip was used to screen the differential expression gene before and after processing, the Real-time PCR technique was used to identify IGFBP3, MALAT1, SOX4, and NDRG1, and the Western blotting detected the level of protein expression of NDRG1, which belongs to up-regulated gene. Results The gene expression spectra chip test showed that there were 161 up-regulated expression gene of colorectal cancer (the fold change was larger than 2), and 64 down-regulated expression genes (the fold change was less than 0.5) after chlorogenic acid treatment. Also, these genes were mainly related to the function of cell signal transduction, biological process and cellular component. The results of Real time PCR showed that the mRNA expression of IGFBP3 and NDRG1 were up-regulated significantly (P < 0.05) after chlorogenic acid treatment. Western Blotting results showed that the NDRG1 gene protein expression was up-regulated significantly (P < 0.05) after chlorogenic acid treatment. Conclusion The gene expression spectrum chip combined the Real-time PCR technology, which were used to screen the differential expression gene before and after the chlorogenic acid treatment, in order to reveal the inhibition mechanism of chlorogenic acid for colorectal cancer cells.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Traditional and Herbal Drugs Ano de publicação: 2017 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Traditional and Herbal Drugs Ano de publicação: 2017 Tipo de documento: Artigo