The effect of overexpression of the HOXD10 gene on the malignant proliferation, invasion, and tumor formation of pancreatic cancer cell PANC-1.

Abstract

To determine the role of HOXD10 in pancreatic cancer. A stable HOXD10-expressing PANC-1 cell line was established. Proliferation rates were detected by 5-Ethynyl-2'-deoxyuridine (Edu) staining while invasion was evaluated by Transwell assay. The expression levels of different proteins were analyzed by Western blotting. A subcutaneous xenograft of pancreatic cancer was established in nude mice, and the tumor weight and body weight were monitored. The in-situ expression of relevant markers in the tumor tissues was detected by immunohistochemistry. HOXD10 overexpression significantly decreased the proliferation rates of PANC-1 cells, and down-regulated Ki67 and Survivin (P<0.05). In addition, the invasive capacity (P<0.05) and the levels of vascular endothelial growth factor (VEGF) and MMP-14 were also significantly decreased (P<0.05) in the cells overexpressing HOXD10. Consistent with this, high levels of HOXD10 were associated with an increase in E-cadherin (P<0.05) and a decrease in N-cadherin (P<0.05) expression. Furthermore, the HOXD10-overexpressing xenografts were significantly smaller (P<0.05) and had fewer Ki67, VEGF, and N-cadherin-positive cells (P<0.05). HOXD10 acts as a tumor suppressor in pancreatic cancer, and inhibits the proliferation, invasion, and epithelial-mesenchymal transition of the tumor cells.