کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2816125 1159916 2014 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
The regulation of ERK and p-ERK expression by cisplatin and sorafenib in gastric cancer cells
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی ژنتیک
پیش نمایش صفحه اول مقاله
The regulation of ERK and p-ERK expression by cisplatin and sorafenib in gastric cancer cells
چکیده انگلیسی


• Cisplatin and sorafenib inhibited gastric cell growth and induced apoptosis.
• Inhibited MKN-45 cell proliferation and induced G0/G1 phase arrest
• Cisplatin and sorafenib promoted the phosphorylation ERK.
• Cisplatin and sorafenib played a synergistic antitumor effect.
• Cisplatin and sorafenib play the antitumor activity by suppressing ERK pathway.

Previous studies have reported strong antitumor effects of cisplatin and sorafenib. Our results indicated that cisplatin and sorafenib exhibited anti-tumor effects on gastric cancer cells. They significantly inhibited gastric cell growth and induced apoptosis. They effectively inhibited gastric cancer cell proliferation and induced G0/G1 phase arrest. Western blotting analysis indicated that it also promoted the phosphorylation extracellular signal regulated kinase (p-ERK). Moreover, cisplatin and sorafenib played a synergistic antitumor effect. These results suggested that the antitumor mechanism of cisplatin and sorafenib involved altering the cell cycle and stimulating ERK phosphorylation in the ERK signaling pathway.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gene - Volume 552, Issue 1, 15 November 2014, Pages 106–115
نویسندگان
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