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 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. Methods 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 . Results 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. Conclusion 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.