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.
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.
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.