Mometasone furoate inhibits the progression of head and neck squamous cell carcinoma via regulating PTPN11

Abstract

Abstract Background: Mometasone Furoate (MF) is a kind of glucocorticoid with extensive pharmacological action including inhibiting tumor progression, however, the role of MF in head and neck squamous cell carcinoma (HNSCC) was still unclear. This study was aim to evaluate the inhibitory effect of MF against HNSCC and investigate the underlying mechanism. Methods: Cell viability, colony formation, cell cycle and cell apoptosis were detected to explore the effect of MF on HNSCC cells. Xenograft study model was conducted to investigate the effect of MF on HNSCC in vivo. The core target of MF against HNSCC was identified by network pharmacology analysis, TCGA database analysis and real-time PCR. Molecular docking was performed to detect the binding energy. Protein tyrosine phosphatase non-receptor type 11 (PTPN11) overexpressed cells were constructed and then cell viability and the expression levels of proliferation- and apoptosis-related proteins were detected after treated with MF to explore the role of PTPN11 in the inhibitory of MF against HNSCC. Results: After cells treated with MF, cell viability and the number of colonies were decreased, cell cycle was arrested and cell apoptosis was increased. Xenograft study results showed that MF could inhibit cell proliferation via promoting cell apoptosis in vivo. PTPN11 was the core target of MF against HNSCC via network pharmacology analysis, TCGA database analysis and real-time PCR. Molecular docking results revealed PTPN11 exhibited the strongest binding ability to MF. Finally, MF could attenuate the effect of increased cell viability and decreased cell apoptosis caused by PTPN11 overexpression, suggesting that MF could inhibit the progression of HNSCC by regulating PTPN11. Conclusion: MF targeted PTPN11 to promote cycle arrest and cell apoptosis subsequently performed an effective anti-tumor activity.