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Hepatocyte growth factor promotes cell survival by phosphorylation of BAD in gastric cancer cells.

机译:肝细胞生长因子通过胃癌细胞中BAD的磷酸化促进细胞存活。

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Hepatocyte growth factor (HGF) is one of the survival factors with a potent ability to promote cell survival by inhibiting apoptosis. However, the mechanism by which HGF inhibits apoptosis is not completely understood. To explore the genes associated with stomach cancer cell survival by HGF, we used cDNA microarray technology and selected 26 genes up- or downregulated in NUGC-3 cells during HGF treatment. Among them, BAD was confirmed to be upregulated at the RNA and protein levels by HGF treatment. We investigated the effect of BAD induced by HGF on cell survival. HGF treatment inhibited apoptosis induced by BAD overexpression and enhanced BAD phosphorylation. Pretreatment of NUGC-3 cells with PI3K inhibitors, LY 294002, decreased HGF-induced BAD phosphorylation on Ser136 whereas an MEK inhibitor, PD 98059, decreased BAD phosphorylation on Ser112. In conclusion, increases in BAD levels as well as BAD phosphoryation by HGF might contribute to HGF-mediated cell survival in NUGC-3 cells.
机译:肝细胞生长因子(HGF)是一种存活因子,具有通过抑制细胞凋亡来促进细胞存活的强大能力。但是,尚不完全了解HGF抑制细胞凋亡的机制。为了探索HGF与胃癌细胞存活相关的基因,我们使用了cDNA微阵列技术,并选择了在HGF治疗期间NUGC-3细胞上调或下调的26个基因。其中,通过HGF处理已确认BAD在RNA和蛋白质水平上调。我们调查了由HGF诱导的BAD对细胞存活的影响。 HGF处理抑制BAD过表达诱导的凋亡,并增强BAD磷酸化。用PI3K抑制剂LY 294002预处理NUGC-3细胞可降低HGF诱导的Ser136上的BAD磷酸化,而MEK抑制剂PD 98059则可降低Ser112上的BAD磷酸化。总之,HGF的BAD水平升高和BAD磷酸化可能有助于NUGC-3细胞中HGF介导的细胞存活。

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