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

• Published in: BMC oral health Vol. 23; no. 1; p. 519
• Main Authors: Li, Liang, Chen, Lihui, Li, Zhangwei, Huang, Shiqin, Chen, Yaoyao, Li, Zhiyong, Chen, Wenkuan
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 25.07.2023; BioMed Central; BMC
• Subjects: Actin; AKT; AKT protein; Carcinogenesis; Care and treatment; Cell adhesion & migration; Cell culture; Cell proliferation; Cholecystokinin; Colonies; Diagnosis; Dosage and administration; Experiments; FSCN1; Glucose; Glucose metabolism; Glycolysis; Health aspects; Interferon; Interferon regulatory factor; Interferon regulatory factor 4; Invasion; IRF4; Liver cancer; Medical prognosis; Metabolism; Metastasis; Mortality; Mouth cancer; Oral cancer; Oral carcinoma; Oral squamous cell carcinoma; OSCC; Proliferation; Proteins; Signal transduction; Software; Squamous cell carcinoma; Therapeutic targets; Tumorigenesis; Western blotting; China; United States > US; OSCC; IRF4; FSCN1; Glycolysis; AKT; Proliferation; Invasion
• ISSN: 1472-6831; 1472-6831
• DOI: 10.1186/s12903-023-03191-9

Oral squamous cell carcinoma (OSCC) is a disease with increasing incidence worldwide that leads to deformity and death. In OSCC, fascin actin-bundling protein 1 (FSCN1) is an oncogene involved in the tumorigenesis process. However, the functions and potential mechanisms of FSCN1 in the OSCC tumorigenesis process have not been reported thus far. We used qRT‒PCR to detect the expression of FSCN1 in 40 paired OSCC tumor tissues (tumor) and neighboring noncancerous tissues. The role of FSCN1 was also assessed in vitro through colony formation, CCK-8, and transwell assays. Moreover, glucose consumption was detected. Western blotting was used to confirm the interaction of FSCN1, IRF4 and AKT. FSCN1 was remarkably overexpressed in OSCC tissues and cell lines compared to corresponding controls. In addition, colony formation, CCK-8, and transwell assays revealed a notable reduction in OSCC growth and invasion when FSCN1 was silenced. FSCN1 silencing remarkably suppressed OSCC glycolysis. Mechanistic studies showed that FSCN1 achieves its function partially by activating interferon regulatory factor 4 (IRF4) and the AKT pathway in OSCC. In conclusion, our study investigated the functions and mechanisms of the FSCN1/IRF4/AKT pathway in OSCC progression. In OSCC, FSCN1 is likely to be a biomarker and therapeutic target.