[IRE1在维生素E琥珀酸盐诱导胃癌细胞自噬中的作用]。

Xue Feng, Bitong Li, Haixia Zhao, Xiaoyang Duan, Yidan Wang, Liying Hou
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引用次数: 0

摘要

目的:探讨肌醇要求酶1(IRE1)在维生素E琥珀酸盐(VES)诱导人胃癌细胞自噬中的作用。方法:体外培养人胃癌SGC-7901细胞,分为溶剂对照组(0.1%无水乙醇)、不同剂量(5、10、15、20 μg/mL) VES组、4μ8C组和VES + 4μ8C组。Western blot检测溶剂对照组和不同剂量VES组内质网应激相关分子葡萄糖调节蛋白78(GRP78)和C/EBP同源蛋白(CHOP)、自噬标志物微管相关蛋白1轻链3(LC3)、Beclin-1、未折叠蛋白反应分支通路肌醇要求酶1(IRE1)、X盒结合蛋白1(XBP1)、C - jun n-末端激酶(JNK)和p-JNK。IRE1被4μ8C抑制。Western blot检测IRE1、XBP1、JNK、p-JNK、GRP78、CHOP的表达,LC3、Beclin-1的表达。结果:20 μg/mL VES组GRP78(1.16±0.06)和CHOP(1.36±0.11)的表达量显著高于溶剂对照组GRP78(0.36±0.10)和CHOP(0.48±0.05)(P<0.001)。20 μg/mL VES组Beclin-1(1.09±0.20)和LC3-Ⅱ/LC3-Ⅰ(1.29±0.03)的表达量显著高于溶剂对照组(0.27±0.07)和LC3-Ⅱ/LC3-Ⅰ(0.43±0.06)(P<0.001)。20 μg/mL VES组IRE1(1.07±0.20)、XBP1(1.33±0.07)、p-JNK/JNK(1.19±0.31)表达量显著高于溶剂对照组(P<0.01)。IRE1抑制后:IRE1(0.63±0.27)、XBP1(0.74±0.09)、p-JNK/JNK(0.35±0.04)、GRP78(0.66±0.02)、CHOP(0.51±0.02)、LC3-Ⅱ/LC3-Ⅰ(0.72±0.01)、Beclin-1(0.70±0.15)表达水平显著低于VES组(P<0.05)。结论:VES可能通过上调IRE1通路参与胃癌细胞自噬的调控。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Role of IRE1 in autophagy induced by vitamin E succinate in human gastric cancer cell].

Objective: To investigate the role of inositol-requiring enzyme 1(IRE1) in autophagy of human gastric cancer cells induced by vitamin E succinate(VES).

Methods: Human gastric cancer SGC-7901 cells were cultured in vitro and divided into solvent control group(0.1% ethanol absolute), different doses(5, 10, 15 and 20 μg/mL) VES group, 4μ8C group, and VES + 4μ8C group. The endoplasmic reticulum stress-related molecules glucose regulated protein 78(GRP78) and C/EBP homologous protein(CHOP), autophagy marker microtubule associated Protein1 light chain 3(LC3), Beclin-1, unfolded protein response branching pathway Inositol-requiring enzyme 1(IRE1), X box-binding protein 1(XBP1), c-Jun n-terminal kinase(JNK) and p-JNK were detected by Western blot in the solvent control group and different doses of VES group. IRE1 was inhibited by 4μ8C. The expressions of IRE1, XBP1, JNK, p-JNK, GRP78 and CHOP were detected by Western blot, and the expressions of LC3 and Beclin-1 were detected.

Results: The expression of GRP78(1.16±0.06) and CHOP(1.36±0.11) in 20 μg/mL VES group were significantly higher than those in solvent control group GRP78(0.36±0.10) and CHOP(0.48±0.05)(P<0.001). The expression of Beclin-1(1.09±0.20) and LC3-Ⅱ/LC3-Ⅰ(1.29±0.03) in 20 μg/mL VES group were significantly higher than those in solvent control group(0.27±0.07) and LC3-Ⅱ/LC3-Ⅰ(0.43±0.06)(P<0.001). The expression levels of IRE1(1.07±0.20), XBP1(1.33±0.07) and p-JNK/JNK(1.19±0.31) in 20 μg/mL VES group were significantly higher than those in the solvent control group(P<0.01). After IRE1 is inhibited: The expression level of IRE1(0.63±0.27), XBP1(0.74±0.09), p-JNK/JNK(0.35±0.04), GRP78(0.66±0.02), CHOP(0.51±0.02), LC3-Ⅱ/LC3-Ⅰ(0.72±0.01), Beclin-1(0.70±0.15) was significantly lower than that of VES group(P<0.05).

Conclusion: VES may participate in the regulation of autophagy in gastric cancer cells by upregulating IRE1 pathway.

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