title: Apoptosis initiation of β-ionone in SGC-7901 gastric carcinoma cancer cells via a PI3K-AKT pathway.
abstract: β-ionone has been shown to hold potent anti-proliferative and apoptosis induction properties in vitro and in vivo. To investigate the effects of β-ionone on apoptosis initiation and its possible mechanisms of action, we qualified cell apoptosis, proteins related to apoptosis and a phosphatidylinositol 3-kinase (PI3K)-AKT pathway in human gastric adenocarcinoma cancer SGC-7901 cells. The results demonstrated that β-ionone-induced apoptosis in a dose-dependent manner in SGC-7901 cells treated with β-ionone (25, 50, 100 and 200 μmol/L) for 24 h. β-ionone was also shown to induce the expression of cleaved-caspase-3 and inhibit bcl-2 expression in SGC-7901 cells in a dose-dependent manner. The significantly decreased levels of p-PI3K and p-AKT expression were observed in SGC-7901 cells after β-ionone treatments in a time- and dose-dependent manner (P < 0.01). Thus, the apoptosis induction in SGC-7901 cells by β-ionone may be regulated through a PI3K-AKT pathway. These results demonstrate a potential mechanism by which β-ionone to induce apoptosis initiation in SGC-7901 cells.
authors.affiliation: Department of Pediatric Surgery, GanNan Medical University, 1 YiXueYuan Road, GanZhou, 341000, Jiangxi, People's Republic of China, liuqian_the1st@yahoo.com.
authors.forename: Qian
authors.initials: Q
authors.lastname: Liu
authors.forename: Hong-Wei
authors.initials: HW
authors.lastname: Dong
authors.forename: Wen-Guang
authors.initials: WG
authors.lastname: Sun
authors.forename: Ming
authors.initials: M
authors.lastname: Liu
authors.forename: Juan C
authors.initials: JC
authors.lastname: Ibla
authors.forename: Lian-Xin
authors.initials: LX
authors.lastname: Liu
authors.forename: John W
authors.initials: JW
authors.lastname: Parry
authors.forename: Xiao-Hui
authors.initials: XH
authors.lastname: Han
authors.forename: Ming-Song
authors.initials: MS
authors.lastname: Li
authors.forename: Jia-Ren
authors.initials: JR
authors.lastname: Liu
mesh_terms: D000230:Adenocarcinoma / Q000201:enzymology* / Q000473:pathology; D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D045744:Cell Line, Tumor; D053144:Cell Nucleus Shape / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D006801:Humans; D045792:Norisoprenoids / Q000494:pharmacology*; D058539:Phosphatidylinositol 3-Kinase / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D013274:Stomach Neoplasms / Q000201:enzymology* / Q000473:pathology; D013997:Time Factors
chemical_list: D000970:Antineoplastic Agents; D045792:Norisoprenoids; D019253:Proto-Oncogene Proteins c-bcl-2; C008157:beta-ionone; D058539:Phosphatidylinositol 3-Kinase; D051057:Proto-Oncogene Proteins c-akt; C505407:CASP3 protein, human; D053148:Caspase 3