MiR-210 knockdown promotes the development of pancreatic cancer via upregulating E2F3 expression

F.-B. Sun, Y. Lin, S.-J. Li, J. Gao, B. Han, C.-S. Zhang

Department of Hepatobiliary Surgery, the Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. zhangyhd@outlook.com

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• Oncology

OBJECTIVE: The aim of this study was to explore the role of microRNA-210 (miR-210) and E2F3 in the development of pancreatic cancer and to investigate the possible underlying mechanism.

PATIENTS AND METHODS: The expression level of miR-210 in pancreatic cancer tissues, para-cancerous tissues, and normal pancreatic tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between miR-210 expression and pathological indicators of pancreatic cancer was analyzed. Meanwhile, the expression of miR-210 in pancreatic cancer cells and normal pancreatic ductal epithelial cells was detected by qRT-PCR. After transfection with miR-210 mimics and inhibitor, the viability and cell cycle of pancreatic cancer cells were detected by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The binding condition of miR-210 and E2F3 was verified by Dual-Luciferase reporter gene assay.

RESULTS: MiR-210 was lowly expressed in pancreatic cancer tissues than that of para-cancerous tissues. The expression of miR-210 was negatively correlated with TNM stage and tumor size of pancreatic cancer. In vitro experiments showed that the miR-210 was downregulated in pancreatic cancer cells than that of normal pancreatic ductal epithelial cells. Meanwhile, overexpression of miR-210 arrested cell cycle decreased cell viability and downregulated E2F3 expression in pancreatic cancer cells. Dual-Luciferase reporter gene assay indicated that E2F3 bound to mi-210. Further experiments confirmed that E2F3 was negatively regulated by miR-210.

CONCLUSIONS: MiR-210 knockdown promotes cell proliferation by upregulating E2F3 expression, thereby promoting the progression of pancreatic cancer.

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