Inhibition of the EP300/Notch Signaling Pathway Regulates Proliferation and Apoptosis in Oral Squamous Cell Carcinoma.

OBJECTIVE

Oral squamous cell carcinoma (OSCC) is highly recurrent and metastatic; EP300 drives tumorigenesis, but its mechanism is unclear.

MATERIALS AND

METHODS

EP300 expression was profiled in OSCC via databases, RT-PCR, and Western blot. Knockdown effects on proliferation (CCK-8, colony), cell cycle, and apoptosis (flow cytometry) were measured. EP300-Notch interplay was probed with Valproic acid, a Notch signaling activator (VPA) rescue assays.

RESULTS

Our experimental results showed that EP300 was upregulated in OSCC Cell Lines. In addition, bioinformatics analysis showed that EP300 upregulation was significantly associated with poor prognosis of OSCC. Prior research and bioinformatics analyses have demonstrated a close relationship between EP300 and the activation of the notch signaling pathway in OSCC. After EP300 knockdown in OSCC cells treated with VPA, our results indicated that VPA could partially reverse the effects of EP300 knockdown on cell proliferation, cell cycle, apoptosis, and EMT processes in OSCC Cells.

CONCLUSION

In this study, we observed that EP300 knockdown suppressed the Notch signaling pathway, consequently inhibiting OSCC cell proliferation, the cell cycle, and EMT while also promoting apoptosis. These findings suggest that EP300 is crucial for OSCC cell growth and development.