PI3K/Akt信号通路对胃癌细胞中PRAS40Thr246磷酸化的影响
Effect of PI3K/Akt Signaling Pathway on PRAS40Thr246 Phosphorylation in Gastric Cancer Cells.
作者信息
Lu Yizhuo, Li Lianghui, Wu Guoyang, Zhuo Huiqin, Liu Guoyan, Cai Jianchun
机构信息
Department of General Surgery, Zhongshan Hospital, Xiamen University, Xiamen, P.R. China.
Institute of Gastrointestinal Oncology, School of Medcine, Xiamen University, Xiamen, P.R. China.
出版信息
Iran J Public Health. 2019 Dec;48(12):2196-2204.
BACKGROUND
We aimed to investigate the effect of PI3K/Akt signaling pathway on PRAS40Thr246 phosphorylation in gastric cancer cells.
METHODS
The study was conducted from April 2017 to January 2018 in Zhongshan Hospital, Xiamen University, Xiamen, China. Gastric cancer cells were divided into three groups: gastric cancer cell group, LY294002 group and MK-2206 group. Specific tests were conducted accordingly.
RESULTS
Inhibition of PI3K/Akt signaling pathway activation and PRAS40Thr246 phosphorylation could inhibit proliferation and invasion and promote apoptosis of gastric cancer cells, and PRAS40Thr246 phosphorylation could activate PI3K/Akt signaling pathway.
CONCLUSION
The levels of PI3K/Akt signaling pathway related proteins and p-PRAS40Thr246 were significantly increased in gastric cancer cells. p-PRAS40-Thr246 was able to reflect the activation of the PI3K/Akt signaling pathway, reflecting the sensitivity of the PI3K/AKT signaling pathway to inhibitors.
背景
我们旨在研究PI3K/Akt信号通路对胃癌细胞中PRAS40苏氨酸246位点磷酸化的影响。
方法
本研究于2017年4月至2018年1月在厦门大学附属中山医院（中国厦门）开展。胃癌细胞被分为三组：胃癌细胞组、LY294002组和MK-2206组。并据此进行了特定检测。
结果
抑制PI3K/Akt信号通路激活和PRAS40苏氨酸246位点磷酸化可抑制胃癌细胞的增殖和侵袭并促进其凋亡，且PRAS40苏氨酸246位点磷酸化可激活PI3K/Akt信号通路。
结论
胃癌细胞中PI3K/Akt信号通路相关蛋白及p-PRAS40苏氨酸246位点水平显著升高。p-PRAS40-苏氨酸246能够反映PI3K/Akt信号通路的激活情况，体现PI3K/AKT信号通路对抑制剂的敏感性。
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