Panoply™ Human PTPN11 Over-expressing Stable Cell Line

Mometasone furoate (MF) is a glucocorticoid with broad pharmacological activity, including inhibiting tumor progression. However, the role of MF in head and neck squamous cell carcinoma (HNSCC) remains unclear. Here, researchers evaluated the inhibitory effect of MF on HNSCC and explored its potential mechanism. MF treatment of cells resulted in decreased cell viability and colony formation, cell cycle arrest, and increased apoptosis. Xenograft tumor experiments showed that MF can inhibit in vivo cell proliferation by promoting apoptosis. Network pharmacology analysis, TCGA database analysis, and real-time quantitative PCR confirmed that protein tyrosine phosphatase non-receptor type 11 (PTPN11) is the core target of MF in its anti-HNSCC activity. Molecular docking results showed that PTPN11 has the strongest binding affinity to MF. Finally, MF attenuated the effects of PTPN11 overexpression on increased cell viability and decreased apoptosis, indicating that MF can inhibit HNSCC progression by regulating PTPN11. MF targets PTPN11, promoting cell cycle arrest and apoptosis, thereby exerting effective anti-tumor activity.

To investigate whether PTPN11 inhibition is a necessary condition for MF to exert its anti-tumor effect, researchers constructed stable PTPN11-overexpressing cells (Figure 1A-C). Interestingly, the expression level of PTPN11 in MF-treated cells was significantly reduced. However, compared with control cells, the expression level of PTPN11 was still relatively high (Figure 1A-C), indicating that MF cannot completely inhibit the overexpression of PTPN11. The cell viability of PTPN11-overexpressing cells was significantly higher than that of control cells, indicating that PTPN11 can promote the proliferation of head and neck squamous cell carcinoma (HNSCC) cells (Figure 1D). After MF treatment, the cell viability of both control and PTPN11-overexpressing cells was significantly reduced, and the cell viability of control cells was slightly lower than that of PTPN11-overexpressing cells, indicating that PTPN11 plays a central role in the inhibitory effect of MF on cell proliferation. Western blotting experiments also observed similar results: after MF treatment, the protein expression levels of Ki67, PCNA, and Bcl-2 in control cells were slightly lower than those in PTPN11-overexpressing cells (Figure 1E and F). Therefore, MF can exert its anti-tumor activity by targeting PTPN11.

Figure 1. MF inhibited the HNSCC progression induced by PTPN11 overexpression. (Qiu, Lin, et al., 2023)