Effect of vitamin E succinate-induced endoplasmic reticulum stress to activate JNK expression on autophagy in human gastric cancer SGC-7901 cells
DOI: 10.3872/j.issn.1007-385x.2021.02.002
- VernacularTitle:维生素E 琥珀酸酯诱导内质网应激激活JNK 的表达对人胃癌SGC-7901
- Author:
CAO Xiaoqiana
1
;
YUAN, Jinhuia
1
;
DU Meizhia
1
;
WANG Yidanb
2
;
HOU Liyinga
1
Author Information
1. a. School of Public Health
2. b. School of Science, North China University of Science and Technology, Tangshan 063020, Hebei, China
- Publication Type:Journal Article
- From:
Chinese Journal of Cancer Biotherapy
2021;28(2):109-114
- CountryChina
- Language:Chinese
-
Abstract:
[Abstract] Objective: To study the role of c-Jun N-terminal kinase (JNK) in vitamin E succinate (VES) activating endoplasmic
reticulum stress-induced autophagy in human gastric SGC-7901 cells. Methods: SGC-7901 cells were treated with different doses of
VES (5, 10, 15, 20 μg/ml) for 24 h, then, qPCR and WB were used to detect the mRNA and protein expressions of autophagy markers
LC3 and Beclin-1; Under the action of reticulum stress inhibitor 4-PBA, the fluorescence intensity and distribution of LC3 were
observed under laser confocal microscope, and then qPCR was used to detect the mRNA expression of endoplasmic reticulum stress
markers GRP78, GRP94 and autophagy markers LC3, Beclin-1. Under the action of the JNK inhibitor SP600125, WB was used to
detect the protein expression changes of p-JNK and autophagy marker proteins LC3 and Beclin-1. Results: Compared with the control
group, with the increase of the concentration of VES, the mRNA and protein expressions of Beclin-1 and LC3 showed a gradual
increase (all P < 0.05), and LC3-Ⅱ/LC3-Ⅰ ratio also increased significantly (P < 0.01); compared with 20 μg/ml VES group, after
pretreatment with endoplasmic reticulum stress inhibitor 4-PBA, mRNA expressions of GRP78, GRP94, LC3 and Beclin-1 decreased
(all P < 0.01), and the intensity of LC3 punctate aggregation decreased; after pretreatment with JNK inhibitor SP600125, the protein
expression levels of p-JNK, LC3 and Beclin-1 were lower than those of 20 μg/ml VES group (all P < 0.01), these results indicated that
inhibition of JNK activity could inhibit the occurrence of autophagy. Conclusion: VES can induce autophagy in SGC-7901cells by
activating endoplasmic reticulum stress, and JNK participates in the regulation process of endoplasmic reticulum stress on autophagy.
- Full text:zgzlswzlzz-2021-2-109.pdf
