Helicobacter pylori infected gastric epithelial cells bypass cell death pathway through the oncoprotein Gankyrin

Dharmendra Kashyap , Nidhi Varshney , Budhadev Baral , Meenakshi Kandpal , Omkar Indari , Ajay Kumar Jain , Debi Chatterji , Sachin Kumar , Hamendra Singh Parmar , Avinash Sonawane , Hem Chandra Jha
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引用次数: 2

Abstract

H. pylori infection can lead to gastric diseases by modulating the various cellular processes such as cellular stress, apoptosis, autophagy, and metabolic changes. H. pylori exposed gastric epithelial cells bypass the cell death pathways. However, the underlying molecular mechanisms remain in infancy. Herein, we determined that H. pylori infection on gastric epithelial cells bypass the cell death pathway via the modulation of autophagy-related signaling molecules (LC3B and ATG7) through the host-associated oncoprotein Gankyrin. Upregulated expression of Gankyrin further enhanced the various antioxidant (gclm, gclc, sod2, cat, keap1, ant, and hsf1) and autophagy-associated genes’ transcripts (atg5, atg7, lc3b, beclin, and sqstm1). Elevated expression of Gankyrin also modulates the various downstream signaling proteins such as Akt, Beta-catenin, and NFkB. We also observed altered cancerous properties of gastric epithelial cells viz; apoptosis, wound healing, chemoresistance, biomass and membrane potential of mitochondria. Concisely, the study revealed that H. pylori infection promotes GC via autophagy through the modulation of oncoprotein Gankyrin and cellular reactive oxygen species (ROS). Overall, our study demonstrated the antiapoptotic property of H pylori-infected gastric epithelial cells might govern through Gankyrin-directed autophagy.

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幽门螺杆菌感染的胃上皮细胞通过癌蛋白甘肽绕过细胞死亡途径
幽门螺旋杆菌感染可通过调节各种细胞过程,如细胞应激、细胞凋亡、自噬和代谢变化而导致胃部疾病。幽门螺杆菌暴露的胃上皮细胞绕过细胞死亡途径。然而,潜在的分子机制仍处于初级阶段。本研究中,我们确定幽门螺杆菌感染胃上皮细胞通过宿主相关癌蛋白Gankyrin调节自噬相关信号分子(LC3B和ATG7)绕过细胞死亡途径。Gankyrin的上调表达进一步增强了各种抗氧化基因(gclm、gclc、sod2、cat、keap1、ant和hsf1)和自噬相关基因(atg5、atg7、lc3b、beclin和sqstm1)的转录本。Gankyrin的表达升高还可以调节各种下游信号蛋白,如Akt、β -catenin和NFkB。我们还观察到胃上皮细胞癌变特性的改变,即;细胞凋亡,伤口愈合,化疗耐药,生物量和线粒体膜电位。简而言之,该研究揭示了幽门螺杆菌感染通过调节癌蛋白甘肽和细胞活性氧(ROS),通过自噬促进胃癌。总之,我们的研究表明,幽门螺杆菌感染的胃上皮细胞的抗凋亡特性可能是通过甘肽导向的自噬来控制的。
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来源期刊
Advances in cancer biology - metastasis
Advances in cancer biology - metastasis Cancer Research, Oncology
CiteScore
2.40
自引率
0.00%
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0
审稿时长
103 days
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