Effect of endostatin on proliferation, invasion and epithelial-mesenchymal transition of basal cell carcinoma cell A431.

Objective: To investigate the effect of endostatin on the proliferation, invasion and epithelial-mesenchymal transition (EMT) of human basal cell carcinoma (BCC) cells (A431).
Patients and Methods: CCK-8 assay and transwell chamber assay were performed to detect cell proliferation and invasion abilities, respectively. Western blot was performed for the detection of the expressions of EMT-related proteins levels. The therapeutic effect of endostatin on tumor formation was tested using a mouse xenograft model.
Results: After endostatin treatment, transwell assay showed that the number of invasive cells in the observation group and control group were (38.25±8.13) and (98.25±9.14), respectively; the relative expression level of E-cadherin protein in the observation group was (0.34±0.03), which was significantly higher than that in the control group (0.14±0.01); the relative expression levels of N-cadherin protein in the observation group was (0.18±0.05), which was significantly lower than that in the control group (0.43±0.03), (all p<0.05).
Conclusions: The expression levels of Vimentin and Fibronectin proteins were significantly lower, while the expression levels of α-smooth muscle Actin (α-SMA) were significantly higher in the observation group than those in the control group. Treatment with endostatin significantly inhibited tumor growth in the mouse xenograft model. Therefore, endostatin can inhibit the proliferation, invasion and EMT in BCC.