FSCN1 promotes proliferation, migration and glycolysis via the IRF4/AKT signalling pathway in oral squamous cell carcinoma

Abstract

Abstract Background: Oral squamous cell carcinoma (OSCC) is an increasing disease worldwide that leads to lethal and deforming consequences. In OSCC, Fascin actin-bundling protein 1 (FSCN1) is identified as an oncogene involved in the tumorigenesis process. But the functions as well as potential mechanisms of FSCN1 in OSCC tumorigenesis process have not been reported so far. Methods: We used RNA sequencing to detect the expreesion of FSCN1 from 40 paired OSCC tissue specimens (Tumor) and neighboring noncancerous tissue. Further colony formation, CCK-8 as well as transwell assay was performed to demonstrate the role of FSCN1 in vitro. Moreover, glucose consumption was detected. Western blot was used to confirm the interaction of FSCN1, IRF4 and AKT. Results: FSCN1 was remarkably overexpressed in OSCC cell lines as well as tissues. Further colony formation, CCK-8 as well as transwell assay suggested that FSCN1 silencing remarkably dampened OSCC growth and migration. Detection of glycolytic metabolism showed that FSCN1 silence remarkably suppressed OSCC glycolysis. Following mechanism studies revealed that FSCN1 realized its functions in OSCC process partially through the interferon regulatory factor 4 (IRF4) and AKT activation. Conclusion: In conclusion, our study investigated the functions as well as the mechanisms of the FSCN1/IRF4/AKT pathway in OSCC progression. FSCN1 could act as a prospective biologic signature and therapeutic target molecule for OSCC.