title: Involvement of endoplasmic reticulum stress in adenosine-induced human hepatoma HepG2 cell apoptosis.
abstract: 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.
authors.affiliation: Department of Gastroenterology, Second Affiliated Hospital, Shantou University Medical College, Shantou 515041, PR China. lingfeiwu@21cn.com
authors.forename: Ling-Fei
authors.initials: LF
authors.lastname: Wu
authors.forename: Yan-Qing
authors.initials: YQ
authors.lastname: Ye
authors.forename: Guan-You
authors.initials: GY
authors.lastname: Huang
authors.forename: Hong-Biao
authors.initials: HB
authors.lastname: Li
authors.forename: Guo-Ping
authors.initials: GP
authors.lastname: Li
authors.forename: Ze-Jin
authors.initials: ZJ
authors.lastname: Pu
authors.forename: Bi-Liu
authors.initials: BL
authors.lastname: Wei
authors.forename: Jia-Lin
authors.initials: JL
authors.lastname: Feng
mesh_terms: D000241:Adenosine / Q000378:metabolism / Q000494:pharmacology; D017209:Apoptosis; D006528:Carcinoma, Hepatocellular / Q000378:metabolism*; D053148:Caspase 3 / Q000378:metabolism*; D053471:Caspases, Initiator / Q000378:metabolism*; D049109:Cell Proliferation; D004305:Dose-Response Relationship, Drug; D004721:Endoplasmic Reticulum / Q000473:pathology*; D000091342:Endoplasmic Reticulum Chaperone BiP; D015972:Gene Expression Regulation, Neoplastic; D006360:Heat-Shock Proteins / Q000378:metabolism*; D056945:Hep G2 Cells; D006801:Humans; D008113:Liver Neoplasms / Q000378:metabolism*; D013778:Tetrazolium Salts / Q000494:pharmacology; D013844:Thiazoles / Q000494:pharmacology; D051742:Transcription Factor CHOP / Q000378:metabolism*
chemical_list: D000091342:Endoplasmic Reticulum Chaperone BiP; D006360:Heat-Shock Proteins; D013778:Tetrazolium Salts; D013844:Thiazoles; D051742:Transcription Factor CHOP; C093516:CASP4 protein, human; D053148:Caspase 3; D053471:Caspases, Initiator; C022616:thiazolyl blue; D000241:Adenosine