Abstract
Mcl-1 expression in gastric cells co-cultured with strain 7.13, consistent with the marked downregulation of miR-320. To define the effect of the H. pylori oncoprotein CagA on these events, cells were also co-cultured with a 7.13 cagAisogenic mutant. Loss of cagA attenuated both the reduction of miR-320 and the subsequent increase in Mcl-1 expression observed in response to wild-type strain 7.13. In summary,H. pylori strain 7.13 specifically downregulates miR-320 in a CagA-dependent manner, which relieves repression of Mcl-1. Upregulation of Mcl-1 by this carcinogenic strain ofH. pylori likely promotes cell survival through inhibition of apoptosis, which may heighten retention of mutagenized cells and increase the risk of subsequent gastric carcinogenesis.
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