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首页> 外文期刊>Gene: An International Journal Focusing on Gene Cloning and Gene Structure and Function >The regulation of ERK and p-ERK expression by cisplatin and sorafenib in gastric cancer cells
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The regulation of ERK and p-ERK expression by cisplatin and sorafenib in gastric cancer cells

机译:顺铂和索拉非尼在胃癌细胞中调节ERK和P-ERK表达

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摘要

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.
机译:先前的研究报告了顺铂和索拉非尼的强烈抗肿瘤作用。 我们的结果表明,顺铂和索拉非尼对胃癌细胞表现出抗肿瘤作用。 它们显着抑制胃细胞生长和诱导的凋亡。 它们有效抑制胃癌细胞增殖并诱导G0 / G1相捕捉。 蛋白质印迹分析表明它还促进了磷酸化细胞外信号调节激酶(P-ERK)。 此外,顺铂和索拉非尼效应了协同抗肿瘤效应。 这些结果表明,顺铂和索拉非尼的抗肿瘤机制涉及改变电池周期并刺激ERK信号通路中的ERK磷酸化。

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