RESUMEN
Tongue squamous cell carcinoma (TSCC) is the most common type of oral squamous cell carcinoma (OSCC) with high morbidity and mortality. Many studies have shown that microRNA (miRNA) are small non-coding RNA that regulate the post-transcriptional processing of target genes, resulting in the degradation and translation inhibition of target mRNA. However, how the transmembrane p24 trafficking protein 2 (TMED2) is regulated by miR-5583-5p on migration, invasion, proliferation and epithelial-mesenchymal transition (EMT) of TSCC Cal-27 cells is unclear. In this study, a database was used to analyze the expression of TMED2 in HNSCC (P <0. 001) in head and neck cancer (HNC). Western blot showed that the expression of TMED2 protein was up-regulated in 6 cases of TSCC tissues and cell lines such as SCC-9, SCC-25 and CAL-27. After the Cal-27 cells transfected with TMED2 interference plasmid (SiTMED2) the expression of E-cadherin was up-regulated, and N-cadherin and Vimentin was down-regulated. Migration and invasion experiments showed that the number of cells transfused into the basement membrane of the cells was lower than that of the control group (P<0. 05). The results of EdU showed that the proliferation of Cal-27 cells transfected with SiTMED2 was decreased (P<0. 05). The results of dual luciferase experiment showed that TMED2 had a binding target to miR-5583-5p, and the expression of miR-5583-5p in Cal-27 cell was lower than that in Hoec cells. The expression of miR-5583-5p was increased and TMED2 protein was decreased after the Cal-27 cells were transfected with miR-5583-5p plasmid (P < 0. 05). In conclusion, TMED2 is regulated by miR-5583-5p and promoted the migration, invasion, proliferation and EMT of tongue squamous cell carcinoma cell Cal-27.
RESUMEN
OBJECTIVES@#A study was conducted to investigate the molecular mechanism of chromodomain helicase/ATPase DNA binding protein 1-like gene (CHD1L) influencing the invasion and metastasis of tongue squamous cell carcinoma and to provide a new target for clinical inhibition of invasion and metastasis of tongue squamous cell carcinoma.@*METHODS@#Ualcan website was used to analyze the expression of CHD1L in normal epithelial tissue and primary head and neck squamous cell carcinoma and to analyze the effect of lymph node metastasis on the expression of CHD1L in tissues with head and neck squamous cell carcinoma. The relationship between CHD1L expression and the survival rate of patients with head and neck squamous cell carcinoma was tested by the GEPIA website. Western blot was used to quantify the levels of CHD1L protein in human tongue squamous cell carcinoma CAL27 and immortalized human skin keratinocyte cell HaCaT. After knocking down CAL27 in human tongue squamous cell carcinoma cells with an RNA interference plasmid, the cells were designated as SiCHD1L/CAL27 and Scr/CAL27. Western blot was utilized to detect the expression of CHD1L in each group of cells. The change in CAL27 cell proliferation ability was tested by EdU proliferation test after CHD1L knockdown. The change of cell migration ability of each group cells was tested through the wound healing assay. Western blot was used to detect epithelial-mesenchymal transition (EMT) marker E-cadherin and Vimentin protein expression levels.@*RESULTS@#Ualcan database showed that the expression of CHD1L in primary head and neck squamous cell carcinoma tissues was higher than in normal epithelial tissues and in head and neck squamous cell carcinoma tissues with lymph node metastasis. GEPIA website analysis showed that the overall survival rate of patients with head and neck squamous cell carcinoma with high expression of CHD1L was significantly lower than that of patients with low expression. Western blot results showed that CHD1L expression in human tongue squamous carcinoma cells CAL27 was higher than that of human normal skin cells HaCaT. CHD1L expression in SiCHD1L/CAL27 cells was much lower than that in Scr/CAL27 cells. Results of EdU proliferation experiments showed the significant reduction in the cell proliferation ability of the SiCHD1L/CAL27 cells. Results of the wound healing experiments showed the reduction in the migration capacity of the SiCHD1L/CAL27 cells. The expression of E-cadherin increased, whereas that of Vimentin decreased, in SiCHD1L/CAL27 cells.@*CONCLUSIONS@#CHD1L promoted the EMT, proliferation, migration, and invasion ability of tongue squamous cell carcinoma cells.