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Mycoplasma hyorhinis infection promotes gastric cancer cell motility via β-catenin signaling.

Research paper by Xia X Liu, Zhuona Z Rong, Chengchao C Shou

Indexed on: 20 Jun '20Published on: 20 Jul '19Published in: Cancer Medicine



Abstract

We previously identified that Mycoplasma hyorhinis infection promotes gastric cancer cell motility. The β-catenin signaling pathway is critical to determining malignant cancer cell phenotypes; however, the association between M hyorhinis and the β-catenin signaling pathway is unclear. We performed subcellular fractionation and immunofluorescence staining to observe β-catenin accumulation in the nucleus. The expression of downstream β-catenin genes was detected by quantitative RT-PCR. Gastric cancer cell motility was examined by transwell chamber migration and wound healing assays, and a co-immunoprecipitation assay was used to detect the proteins associated with the membrane protein p37 of M hyorhinis. We found that M hyorhinis infection promoted nuclear β-catenin accumulation and enhanced the expression of downstream β-catenin genes. M hyorhinis-promoted gastric cancer cell motility was counteracted by treatment with the β-catenin inhibitor XAV939 or β-catenin knockdown. We further detected a protein complex containing LRP6, GSK3β, and p37 in M hyorhinis-infected cells. M hyorhinis also induced LRP6 phosphorylation in a GSK3β-dependent fashion. Knockdown of LRP6 or GSK3β abolished M hyorhinis-induced cell motility. Our results reveal that the β-catenin signaling pathway could be activated by M hyorhinis infection, thereby contributing to M hyorhinis-induced gastric cancer cell motility. © 2019 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.