Involvement of endoplasmic reticulum stress in adenosine-induced human hepatoma HepG2 cell apoptosis
Autor: | Yan-Qing Ye, Hong-Biao Li, Bi-Liu Wei, Ling-Fei Wu, Guo-Ping Li, Guan-You Huang, Ze-Jin Pu, Jia-Lin Feng |
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Rok vydání: | 2011 |
Předmět: |
Cancer Research
Adenosine Carcinoma Hepatocellular Cell Tetrazolium Salts Apoptosis CHOP Biology Endoplasmic Reticulum chemistry.chemical_compound medicine Humans MTT assay DAPI Endoplasmic Reticulum Chaperone BiP Heat-Shock Proteins Cell Proliferation Dose-Response Relationship Drug Caspase 3 Cell growth Liver Neoplasms Hep G2 Cells General Medicine Cell cycle Caspases Initiator Cell biology Gene Expression Regulation Neoplastic Thiazoles medicine.anatomical_structure Oncology chemistry Cytoplasm Transcription Factor CHOP |
Zdroj: | Oncology Reports. |
ISSN: | 1791-2431 1021-335X |
Popis: | Endoplasmic reticulum stress (ERS)-mediated cell apoptosis has been implicated in the development of multiple diseases such as cancer, neurodegenerative diseases and ischemic reperfusion damage. Previous studies have demonstrated the adenosine-induced apoptosis in several tumor cell lines. However, the role of ERS in adenosine-induced human hepatoma HepG2 cell apoptosis remains unclear. The present study was designed to determine whether ERS is involved in adenosine-induced HepG2 cell apoptosis. The MTT assay was used to determine proliferation, and DAPI staining of cell nuclei was performed to determine cell apoptosis. The translocation of CHOP and caspase-3 was observed by immunofluorescence analysis, and the protein expression of CHOP, caspase-4 and caspase-3 was detected by Western blotting. The MTT assay demonstrated that adenosine inhibited HepG2 cell proliferation in a dose-dependent manner. DAPI staining of cell nuclei and cell cycle analysis verified cell apoptosis. The immunofluorescence assay demonstrated that adenosine induced the translocation of CHOP and of caspase-3 from the cytoplasm to the nucleus. Western blotting confirmed that CHOP, caspase-4 and caspase-3 were up-regulated in HepG2 cells after treatment with adenosine. However, JNK protein expression was not altered. These results show that ERS is involved in the adenosine-induced HepG2 cell apoptosis. |
Databáze: | OpenAIRE |
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