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Archived Comments for: Helicobacter pylori virulence factor CagA promotes tumorigenesis of gastric cancer via multiple signaling pathways

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  1. Gastric cancer stem cells induced by H. pylori infection-induced autophagy 

    Go Yoshida, Tokyo Medical and Dental University

    30 July 2015

    Vacuolating cytotoxin A (VacA) in H. pylori-infected gastric cells increases reactive oxygen species (ROS) and induce conventional autophagy, thereby promoting the degradation of PAI-encoded cytotoxin-associated gene A (CagA) protein. Decreased CagA prevents tumorigenesis by inhibiting Src/MEK/ERK signaling activation.

    CD44 variant 8-10 (CD44v)-expressing gastric cells have enhanced anti-ROS machinery via the stabilization of xCT cysteine transporter at the cellular membrane. This CD44v-xCT-glutathione axis results in the accumulation of CagA, which is why CD44v-positive cells are potential gastric tumor-initiating cells.


    Reference; Cell Host & Microbe, 12, 764-777 (2012)

    Competing interests

    There are no competing interests to be addressed.