MYG1 interacts with HSP90 to promote breast cancer progression through Wnt/β-catenin and Notch signaling pathways.

Abstract

Background: As an evolutionarily conserved gene involved in embryonic development, cell differentiation, and immune metabolism, MYG1 exhibits a dynamic expression pattern related to development in human and mouse embryonic tissues, especially upregulates in undifferentiated or pluripotent stem cells. However, MYG1 has been poorly studied in breast cancer and its functional mechanism still remains unclear.

Method: Immunohistochemistry and immunofluorescence were used to study MYG1 expression and localization in breast cancer. Lentivirus transfection combined with CCK8, colony formation, matrix gel experiment and breast fat pad tumor formation in nude mice were used for in vivo and in vitro functional assessment. GSEA enrichment analysis, immunofluorescence and western blot were conducted to explore functional mechanism.

Result: MYG1 expression was upregulated in breast cancer and its higher expression correlated with a variety of clinicopathological characteristics indicating poor prognosis. In vitro and in vivo experiments showed that overexpression of MYG1 promoted breast cancer cells proliferation, migration, invasion and tumorigenesis, while downregulation of MYG1 had an opposite effect. Mechanistically, MYG1 interacted with HSP90 to significantly activate Wnt/β-catenin and Notch signaling pathways in breast cancer cells, thus promoting EMT, cell cycle process and breast cancer progression.

Conclusion: MYG1 is highly expressed in breast cancer and functions as an oncogene. Mechanistically, MYG1 interacts with HSP90 to accelerate EMT and cell cycle process by activating both Wnt/β-catenin and Notch signaling pathways.