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

11Citations
Citations of this article
9Readers
Mendeley users who have this article in their library.

Abstract

Background: To determine the role of HOXD10 in pancreatic cancer. Methods: 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. Results: 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). Conclusions: HOXD10 acts as a tumor suppressor in pancreatic cancer, and inhibits the proliferation, invasion, and epithelial-mesenchymal transition of the tumor cells.

Cite

CITATION STYLE

APA

Lin, Z., Hu, Y., Lin, R., & Ye, H. (2020). The effect of overexpression of the HOXD10 gene on the malignant proliferation, invasion, and tumor formation of pancreatic cancer cell PANC-1. Gland Surgery, 9(2), 385–391. https://doi.org/10.21037/gs.2020.03.28

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free