ABSTRACT
Objective@#To explore the role of apoliprotein D (APOD) in the proliferation and migration of human dental pulp cells (DPCs) and to provide a basis for the use of APOD to promote pulp regeneration. @*Methods@#APOD expression in human dental pulp cells was inhibited by siRNA. The inhibition effect of APOD was confirmed by qPCR and Western blot. After APOD inhibition, colony formation experiments and CCK8 assays were employed to confirm the proliferation ability of dental pulp cells. Transwell assays were used to verify the cell migration ability after the inhibition of APOD expression.@*Results @# After inhibiting APOD expression, the colony formation rate in the si-apod group was reduced compared with the NC group, and the difference was statistically significant (t=7.624, P=0.002). The CCK8 experiment showed that the OD value in the si-apod group decreased at 3, 5 and 7 d compared with that in the NC group (P < 0.05). Transwell results showed that the number of cell divisions was 57.25 ± 4.03 in the si-apod group and 154.50 ± 8.39 in the NC group, and the difference was statistically significant (t=10.45, P < 0.001).@*Conclusion@# Inhibition of APOD expression in dental pulp cells inhibits their proliferation and migration ability.
ABSTRACT
Objective@#To investigate the levels of the Twist and Vimentin proteins in oral squamous cell carcinoma (OSCC) and analyze the clinical significance of Twist and Vimentin.@*Methods@# Eighty-five samples of OSCC and fifteen samples of normal oral mucosa were collected. Immunohistochemistry (SP method) was used to detect the expression of proteins, including Twist and vimentin. The relationship among these proteins and clinical pathological parameters was analyzed using SPSS statistical software.@*Results @#In the normal group, 13.3% (2/15) of samples were positive for the Twist protein; this value was significantly lower than that in OSCC group (80.0%, 66/85) (χ2=26.98, P < 0.001). The expression of Twist was associated with clinical stage (χ2=5.40, P=0.02) and lymph node metastasis (χ2=8.35, P=0.006), while no correlations were found between the expression of Twist and sex (χ2=0.23, P=0.63), age (χ2= 0.31, P=0.58), location (χ2=1.46, P=0.235) or degree of differentiation (χ2=1.52, P=0.47). Additionally, 6.7% of samples (1/15) were positive for vimentin; this value was significantly lower than that in OSCC group (74.1%, 63/85) (χ2=20.71, P < 0.001). The expression of vimentin was associated with clinical stage (χ2=4.51, P=0.034) and lymph node metastasis (χ2=6.75, P=0.009), while no correlations were found between the expression of vimentin and sex (χ2=0.40, P=0.53), age (χ2=0.17, P=0.68), location (χ2=0.74,P=0.39) or degree of differentiation (χ2=4.58, P=0.10). Spearman correlation analyses showed that Twist protein expression was positively correlated with vimentin (r=0.578, P＜0.05). @*Conclusion@#Our data demonstrate that in OSCC, Twist and vimentin levels were upregulated, and Twist protein expression was positively correlated with vimentin, which indicates that both Twist and vimentin may be involved in the occurrence of OSCC.