Expression and function of dinkkopf 4 in oral squamous cell carcinoma and in vitro

Abstract Background Oral squamous cell carcinoma accounts for about 90% of malignant tumors of the head and neck, and its 5-year survival is less than 50%. The number of new cases of oral cancer worldwide is expected to increase by 62% in 2035. Wnt/β-catenin signal pathway plays a role in the tumorigenesis and progression of cancer. dinkkopf 4 is involved in a variety of cancers as a molecule in Wnt/β-catenin signal. To our knowledge, the study of DKK4 in OSCC has not been reported. Methods The well differentiated oral squamous cell carcinoma and normal oral mucosa samples were collected from Department of Pathology of Xiangya Stomatological Hospital of Central South University. Human oral epithelial cell HOEC and human oral squamous cell carcinoma cell TSCC1 were cultured for experiments. The plasmid vector was constructed to inhibit the expression of DKK4 to form TSCC1-shDKK4 cells and TSCC1-NC cells were transfected with blank plasmid. Cell proliferation was detected by CCK-8 test. Apoptosis was detected by Annexin V-FITC/PI assay. Cell migration was detected by Transwell assay. IBM SPSS Statistics 24.0 and GraphPad Prism 8 were performed for statistical analysis and graphing. Results We found that the expression of DKK4 and β-catenin increased in OSCC and in vitro (P<0.05). dinkkopf 4 may promote the expression of β-catenin in OSCC. The proliferation and migration of TSCC1-shDKK4 cells decreased and the apoptosis of TSCC1-shDKK4 cells increased (P<0.01). Conclusions dinkkopf 4 may promote the proliferation and migration of OSCC cells and inhibit the apoptosis of OSCC cells in vitro by regulating Wnt/β-catenin signal pathway.