Protective Macroautophagy Is Involved in Vitamin E Succinate Effects on Human Gastric Carcinoma Cell Line SGC-7901 by Inhibiting mTOR Axis Phosphorylation
Vitamin E succinate (VES), a potential cancer therapeutic agent, potently induces apoptosis and inhibits the growth of various cancer cells. Autophagy has been supposed to promote cancer cell survival or trigger cell death, depending on particular cancer types and tumor microenvironments. The role o...
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Published in | PloS one Vol. 10; no. 7; p. e0132829 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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13.07.2015
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Abstract | Vitamin E succinate (VES), a potential cancer therapeutic agent, potently induces apoptosis and inhibits the growth of various cancer cells. Autophagy has been supposed to promote cancer cell survival or trigger cell death, depending on particular cancer types and tumor microenvironments. The role of autophagy in the growth suppressive effect of VES on gastric cancer cell is basically unknown. We aimed to determine whether and how autophagy affected the VES-induced inhibition of SGC-7901 human gastric carcinoma cell growth. SGC-7901 cells were treated with VES or pre-treated with autophagy inhibitor, chloroquine (CQ) and 3-methyladenine (3-MA). Electron microscopy, fluorescence microscopy and Western blot were used to study whether VES induced autophagy reaction in SGC-7901 cells. Western blot evaluated the activities of the mammalian target of rapamycin (mTOR) axis. Then we used 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry to detect the level of cell viability and apoptosis. Collectively, our data indeed strongly support our hypothesis that VES treatment produced cytological variations that depict autophagy, increased the amount of intracellular green fluorescent protein-microtubule associated protein 1 light chain 3 (GFP-LC3) punctate fluorescence and the number of autophagic vacuoles. It altered the expression of endogenous autophagy marker LC3. VES activated the suppression of mTOR through inhibiting upstream regulators p38 MAPK and Akt. mTOR suppression consequently inhibited the activation of mTOR downstream targets p70S6K and 4E-BP-1. The activation of the upstream mTOR inhibitor AMPK had been up-regulated by VES. The results showed that pre-treatment SGC-7901 with autophagy inhibitors before VES treatment could increase the capacity of VES to reduce cell viability and to provoke apoptosis. In conclusion, VES-induced autophagy participates in SGC-7901 cell protection by inhibiting mTOR axis phosphorylation. Our findings not only strengthen our understanding of the roles of autophagy in cancer biology, but may also be useful for developing new treatments for gastric cancer patients. |
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AbstractList | Vitamin E succinate (VES), a potential cancer therapeutic agent, potently induces apoptosis and inhibits the growth of various cancer cells. Autophagy has been supposed to promote cancer cell survival or trigger cell death, depending on particular cancer types and tumor microenvironments. The role of autophagy in the growth suppressive effect of VES on gastric cancer cell is basically unknown. We aimed to determine whether and how autophagy affected the VES-induced inhibition of SGC-7901 human gastric carcinoma cell growth. SGC-7901 cells were treated with VES or pre-treated with autophagy inhibitor, chloroquine (CQ) and 3-methyladenine (3-MA). Electron microscopy, fluorescence microscopy and Western blot were used to study whether VES induced autophagy reaction in SGC-7901 cells. Western blot evaluated the activities of the mammalian target of rapamycin (mTOR) axis. Then we used 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry to detect the level of cell viability and apoptosis. Collectively, our data indeed strongly support our hypothesis that VES treatment produced cytological variations that depict autophagy, increased the amount of intracellular green fluorescent protein—microtubule associated protein 1 light chain 3 (GFP-LC3) punctate fluorescence and the number of autophagic vacuoles. It altered the expression of endogenous autophagy marker LC3. VES activated the suppression of mTOR through inhibiting upstream regulators p38 MAPK and Akt. mTOR suppression consequently inhibited the activation of mTOR downstream targets p70S6K and 4E-BP-1. The activation of the upstream mTOR inhibitor AMPK had been up-regulated by VES. The results showed that pre-treatment SGC-7901 with autophagy inhibitors before VES treatment could increase the capacity of VES to reduce cell viability and to provoke apoptosis. In conclusion, VES-induced autophagy participates in SGC-7901 cell protection by inhibiting mTOR axis phosphorylation. Our findings not only strengthen our understanding of the roles of autophagy in cancer biology, but may also be useful for developing new treatments for gastric cancer patients. |
Audience | Academic |
Author | Li, Yuze Wu, Kun Song, Huacui Hou, Liying Zhang, Zhihong Zhang, Xuguang Sun, Yanpei |
AuthorAffiliation | 2 Department of the Fourth Internal Medicine, The Fourth Hospital of Heilongjiang Province, Harbin, China 4 Department of Internal Medicine, Hematology and Oncology, Harbin Children’s Hospital, Harbin, China 3 Food Processing Institute, Heilongjiang Academy of Agricultural Sciences, Harbin, China National Cheng Kung University, TAIWAN 1 Department of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, Harbin, China |
AuthorAffiliation_xml | – name: 4 Department of Internal Medicine, Hematology and Oncology, Harbin Children’s Hospital, Harbin, China – name: 1 Department of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, Harbin, China – name: 2 Department of the Fourth Internal Medicine, The Fourth Hospital of Heilongjiang Province, Harbin, China – name: 3 Food Processing Institute, Heilongjiang Academy of Agricultural Sciences, Harbin, China – name: National Cheng Kung University, TAIWAN |
Author_xml | – sequence: 1 givenname: Liying surname: Hou fullname: Hou, Liying organization: Department of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, Harbin, China – sequence: 2 givenname: Yuze surname: Li fullname: Li, Yuze organization: Department of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, Harbin, China; Department of the Fourth Internal Medicine, The Fourth Hospital of Heilongjiang Province, Harbin, China – sequence: 3 givenname: Huacui surname: Song fullname: Song, Huacui organization: Department of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, Harbin, China – sequence: 4 givenname: Zhihong surname: Zhang fullname: Zhang, Zhihong organization: Department of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, Harbin, China; Food Processing Institute, Heilongjiang Academy of Agricultural Sciences, Harbin, China – sequence: 5 givenname: Yanpei surname: Sun fullname: Sun, Yanpei organization: Department of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, Harbin, China – sequence: 6 givenname: Xuguang surname: Zhang fullname: Zhang, Xuguang organization: Department of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, Harbin, China; Department of Internal Medicine, Hematology and Oncology, Harbin Children's Hospital, Harbin, China – sequence: 7 givenname: Kun surname: Wu fullname: Wu, Kun organization: Department of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, Harbin, China |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26168048$$D View this record in MEDLINE/PubMed |
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DocumentTitleAlternate | Vitamin E Succinate Induces Autophagy on SGC-7901 Cell |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: KW LH. Performed the experiments: LH HS YS XZ. Analyzed the data: ZZ. Contributed reagents/materials/analysis tools: YL. Wrote the paper: LH. |
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Snippet | Vitamin E succinate (VES), a potential cancer therapeutic agent, potently induces apoptosis and inhibits the growth of various cancer cells. Autophagy has been... |
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SubjectTerms | Activation AKT protein Apoptosis Autophagy Bromine compounds Cancer Cancer therapies Carcinoma Cell culture Cell death Cell Line, Tumor Cell survival Chemical compounds Chemotherapy Chloroquine Cytometry Drug resistance Electron microscopy Flow cytometry Fluorescence Fluorescence microscopy Food Gastric cancer Green fluorescent protein Health aspects Homeostasis Humans Hygiene Inhibitors Internal medicine Kinases MAP kinase Metabolism Microenvironments Mortality Nutrition Phagocytosis Pharmacology Phosphorylation Proteins Public health Rapamycin Regulators Signal Transduction Stomach cancer Stomach Neoplasms - immunology Stomach Neoplasms - metabolism Stomach Neoplasms - pathology Tocopherol TOR protein TOR Serine-Threonine Kinases - metabolism Upstream Vacuoles Vitamin E Vitamin E - pharmacology |
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Title | Protective Macroautophagy Is Involved in Vitamin E Succinate Effects on Human Gastric Carcinoma Cell Line SGC-7901 by Inhibiting mTOR Axis Phosphorylation |
URI | https://www.ncbi.nlm.nih.gov/pubmed/26168048 https://www.proquest.com/docview/1695995297 https://search.proquest.com/docview/1696683833 https://pubmed.ncbi.nlm.nih.gov/PMC4500415 https://doaj.org/article/0d4c95ac917e4811839b256ac33ea9d3 http://dx.doi.org/10.1371/journal.pone.0132829 |
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