Abstract:

To  investigate the role of endoplasmic reticulum stress protein in oxidative stress-induced autophgy in human cervical carcinoma Hela cells,and to clarify the possible mechanism of endoplasmic reticulum stress-autophagy pathway in regulating the survival of tumor cells.Methods Hela cells were divided into control group,VK3 (30   μmol•L^-1) group，ER stress inhibitor TUDC (500  μmol•L-1) group，VK3(30   μmol•L^-1) +TUDC(500  μmol•L^-1)  group.The morphological changes of endoplasmic reticulum of Hela cells  were observed by transmission electron microscope.The survival rate of Hela cells in each group was measured by MTT assay.The expression levels of glucose-regulated protein-78 (GRP78) and LC3-Ⅱ were determined by Western blotting method.Results The morphology of Hela cells in control group was normal.The autophagic vacuoles and dilated endoplasmic reticulum were observed in cytoplasm of Hela cells in VK3 group.Compared with VK3 group，the survival rate of Hela cells in VK3+ TUDC group was decreased(P<0.05).Compared with control group,the expression levels of GRP78 and LC3-Ⅱ in VK3 group were decreased(P<0.05).Compared with VK3 group,the expression levels of GRP78 and LC3-Ⅱ in TUDC+ VK3 group were decreased (P<0.05).Conclusion Endoplasmic reticulum stress protein can mediate the  autophgy of Hela cells in oxidative stress-induced injury of Hela cells.
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Key words: oxidative stress, endoplasmic reticulum, glucose-regulated protein　78, autophagy, Hela cells