Histone demethylase RBP2 induced by Helicobactor Pylori CagA participates in the malignant transformation of gastric epithelial cells

作者: Xiuming Liang , Jiping Zeng , Lixiang Wang , Li Shen , Shuyan Li

DOI: 10.18632/ONCOTARGET.2185

关键词: HistonePI3K/AKT/mTOR pathwayDemethylaseDownregulation and upregulationCagABiologyHematologyMolecular biologyMalignant transformationInternal medicineCyclin D1Cancer research

摘要: // Xiuming Liang 1 , Jiping Zeng 2 Lixiang Wang 3 Li Shen Shuyan Lin Ma Xinyu Ci Jingya Yu Mutian Jia Yundong Sun Zhifang Liu Shili Wenjuan Han Chunyan Chen 4 and Jihui Department of Microbiology/Key Laboratory for Experimental Teratology Chinese Ministry Education, School Medicine, Shandong University, Jinan, PR China Biochemistry, Pharmacology, Hematology, Qilu Hospital, No.107,Wenhua Xi Road, Jinan 250012, Shandong, P. R. Correspondence: Jia, email: Keywords : RBP2, CagA, GC, Sp1, malignant transformation Received May 17, 2014 Accepted July 06, Published 08, Abstract Gastric epithelial cell induced by Helicobactor Pylori contributes to tumor development, but the underlying mechanisms this remain unclear. Here we demonstrate that a newly identified histone demethylase, can be CagA via PI3K/AKT-Sp1 pathway depending on AKT phosphorylation. Sp1 directly binds RBP2 promoter enhances its expression then upregulated significantly increases Cyclin D1 transcription, which gastric transformation. Further data indicate knockdown endogenous dominantly inhibits cancer (GC) development both in vitro vivo. In conclusion, CagA- PI3K/AKT-Sp1-RBP2-Cyclin may serve as novel mechanism (GC). Therefore, link chronic inflammation inhibition have potential therapeutic advantages.

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