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

Abstract

Background 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. Methods 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. Results 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. Conclusion 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.

Targeting MetaLnc9/miR-143/FSCN1 axis inhibits oxidative stress and myofibroblast transdifferentiation in oral submucous fibrosis

“… 29 Indeed, increased FSCN1 was found to stimulate the invasion, and glycolysis of oral cancer cells via the IRF4/AKT signaling. 30 , 31 Moreover, it has been shown that the elevation of FSCN1 mediated epithelial-to-mesenchymal transition (EMT) since it was a downstream effector of SNAI2 in the TGF-β-induced EMT in human lung and oral cancer cells. 32 , 33 Since cells undergo EMT is a major source of fBMFs, 1 , 6 , 34 , 35 it is reasonable to presume that FSCN1 may contribute to the transdifferentiation of fBMFs.…”

DKK2 promotes the progression of oral squamous cell carcinoma through the PI3K/AKT signaling pathway

“…Malignant tumors originating from squamous cells contribute significantly to oral cancer, comprising over 90% of cases [ 2 ]. HNSCC is the most prevalent malignant tumor in the head and neck region, and its incidence has been gradually increasing in recent years [ 3 ]. HNSCC is a burden faced globally, with a high mortality rate of approximately 500,000 deaths in 2022 due to its characteristics of late diagnosis, rapid local invasion, high metastasis, and difficult management [ 4 ].…”

Integration RNA bulk and single cell RNA sequencing to explore the change of glycolysis-related immune microenvironment and construct prognostic signature in head and neck squamous cell carcinoma

“…In the past, single tumor immunotherapy did not get the desired results, mostly because the inhibitory effect of metabolic reprogramming on immune cells in microenvironment was not taken into account [ 5 ].Abnormal energy metabolism is the basic feature of tumor, and abnormal glucose metabolism is the most important feature of tumor [ 6 ]. Glycolysis was obviously activated in head and neck squamous cell carcinoma, and the increase of key enzymes related to glycolysis occurred in oral squamous cell carcinoma, laryngeal squamous cell carcinoma and pharyngeal carcinoma [ [7] , [8] , [9] ]. The process of glycolysis not only increases energy supply by itself, but also promotes immune escape of tumor cells.…”