title: Diallyl disulfide suppresses proliferation and induces apoptosis in human gastric cancer through Wnt-1 signaling pathway by up-regulation of miR-200b and miR-22.
abstract: The purpose of this study was to identify a mechanism related to miRNA pathway which plays a role in the anti-tumor effects of Diallyl disulfide. Alterations in miRNA expression were observed in Diallyl disulfide-treated MGC-803 cells, including up-regulation of miR-200b and miR-22 expression. Furthermore, Wnt-1 was identified as a target of both miR-200b and miR-22. MiR-200b and miR-22 not only synergistically inhibited gastric cancer growth, but also enhanced the antitumor effect of Diallyl disulfide both in vitro and in vivo. It indicated that miR-200b and miR-22 may serve as potential gene therapy and enhance Diallyl disulfide antitumor effects.
authors.affiliation: Department of Breast Oncology, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, People's Republic of China; State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, People's Republic of China; Cancer Research Institute, University of South China, Hengyang, Hunan, People's Republic of China.
authors.forename: Hailin
authors.initials: H
authors.lastname: Tang
authors.forename: Yanan
authors.initials: Y
authors.lastname: Kong
authors.forename: Jiaoli
authors.initials: J
authors.lastname: Guo
authors.forename: Yi
authors.initials: Y
authors.lastname: Tang
authors.forename: Xinhua
authors.initials: X
authors.lastname: Xie
authors.forename: Lu
authors.initials: L
authors.lastname: Yang
authors.forename: Qi
authors.initials: Q
authors.lastname: Su
authors.forename: Xiaoming
authors.initials: X
authors.lastname: Xie
mesh_terms: D000230:Adenocarcinoma / Q000473:pathology / Q000628:therapy*; D000498:Allyl Compounds / Q000494:pharmacology*; D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D001483:Base Sequence; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D003131:Combined Modality Therapy; D004220:Disulfides / Q000494:pharmacology*; D015972:Gene Expression Regulation, Neoplastic; D015316:Genetic Therapy; D006801:Humans; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D034622:RNA Interference; D013274:Stomach Neoplasms / Q000473:pathology / Q000628:therapy*; D059467:Transcriptome / Q000187:drug effects; D047368:Tumor Burden; D015854:Up-Regulation; D060449:Wnt Signaling Pathway; D051155:Wnt1 Protein / Q000235:genetics / Q000378:metabolism*; D023041:Xenograft Model Antitumor Assays
chemical_list: D000498:Allyl Compounds; D000970:Antineoplastic Agents; D004220:Disulfides; C533896:MIRN200 microRNA, human; C548375:MIRN22 microRNA, human; D035683:MicroRNAs; D051155:Wnt1 Protein; C028009:diallyl disulfide
keywords: Diallyl disulfide; Gastric cancer; MicroRNA; Wnt-1 signaling pathway