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

被引:18
作者
Liu, Xia
Rong, Zhuona
Shou, Chengchao
机构
[1] Peking Univ, Canc Hosp & Inst, Dept Biochem, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing, Peoples R China
[2] Peking Univ, Canc Hosp & Inst, Dept Mol Biol, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing, Peoples R China
基金
中国国家自然科学基金;
关键词
gastric cancer cell; motility; Mycoplasma hyorhinis; beta-catenin; SYNTHASE KINASE 3-BETA; COLORECTAL-CANCER; WNT; EXPRESSION; MUTATIONS; INVASIVENESS; ACTIVATION; TCF; PHOSPHORYLATION; CARCINOMAS;
D O I
10.1002/cam4.2357
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:5301 / 5312
页数:12
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