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

Background We previously identified that Mycoplasma hyorhinis infection promotes gastric cancer cell motility. The beta-catenin signaling pathway is critical to determining malignant cancer cell phenotypes; however, the association between M hyorhinis and the beta-catenin signaling pathway is unclear. Methods We performed subcellular fractionation and immunofluorescence staining to observe beta-catenin accumulation in the nucleus. The expression of downstream beta-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. Results We found that M hyorhinis infection promoted nuclear beta-catenin accumulation and enhanced the expression of downstream beta-catenin genes. M hyorhinis-promoted gastric cancer cell motility was counteracted by treatment with the beta-catenin inhibitor XAV939 or beta-catenin knockdown. We further detected a protein complex containing LRP6, GSK3 beta, and p37 in M hyorhinis-infected cells. M hyorhinis also induced LRP6 phosphorylation in a GSK3 beta-dependent fashion. Knockdown of LRP6 or GSK3 beta abolished M hyorhinis-induced cell motility. Conclusion Our results reveal that the beta-catenin signaling pathway could be activated by M hyorhinis infection, thereby contributing to M hyorhinis-induced gastric cancer cell motility.