Conclusion
Taken together, our results showed for the first time that FOXN2 plays an essential role in cell proliferation and invasion. Thus, FOXN2 may be an attractive therapeutic target for the treatment of breast cancer.
Methods
In the present work, we explored the detailed molecular mechanism of FOXN2 in breast cancer. We performed RT-qPCR and Western blotting analysis to detect the expression of FOXN2 in breast cancer. Colony formation assay, CCK-8 assay, wound healing assay, and Transwell assay were used to determine the effect of FOXN2 on cell proliferation, migration, and invasion in breast cancer.
Results
Our results demonstrated that FOXN2 was downregulated in breast cancer tissues and cell lines. Downregulation of FOXN2 was correlated with tumor size, pathological grade, and lymph node metastasis. The in vitro experiments revealed that the ectopic expression of FOXN2 significantly suppressed the proliferation, migration, and invasiveness of breast cancer cells, and inhibition of FOXN2 promoted the proliferation, migration, and invasiveness of breast cancer cells. Moreover, inhibition of FOXN2 facilitated epithelial-mesenchymal transition (EMT) through regulation of SLUG.