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Article type: Research Article
Authors: Li, Jian-Qiang* | Yang, Xun | Zhou, Xin-Ming
Affiliations: Department of Thoracic Surgery, Zhejiang Cancer Hospital, Hangzhou 310022, Zhejiang, China
Correspondence: [*] Corresponding author: Jian-Qiang Li, Department of Thoracic Surgery, Zhejiang Cancer Hospital, No 38, Banshan Bridge Guangji Road, Gongshu District, Hangzhou 310022, Zhejiang, China. Tel.: +86 0571 88128051; E-mail:[email protected]
Abstract: We aimed to study the effect of PIM1 gene silencing on the proliferation and apoptosis of human esophageal cancer cell line Eca109. Cultured Eca109 cells were transfected with the recombinant plasmids in mediation of Lipofectamine TM 2000 Reagent. The Eca109 cells in logarithmic growth phase were collected and assigned into three groups: the PIM1 siRNA group (stably transfected with PIM1-shRNA plasmids), the negative control (NC) group (transfected with vacant plasmids), and the blank group (Eca109 cells without any transfection). The PIM1 mRNA expression was determined by real-time quantitative polymerase chain reaction (RT-qPCR). Cell cycle was analyzed by flow cytometry. Cell proliferation was evaluated using the Cell Counting Kit-8 (CCK-8). Cell apoptosis was assessed by Annexin V-FITC/PI double-staining and TUNEL assays. The PIM1 mRNA expression of Eca109 cells in the PIM1 siRNA group was significantly lower than that in the NC and blank groups. Compared with the NC and blank groups, the viability and proliferation of the Eca109 cells in the PIM1 siRNA group were significantly decreased at 48 h, 72 h and 96 h after transfection. The cell growth inhibition rate of the PIM1 siRNA group was higher than that of the NC and blank groups after transfection. Furthermore, the apoptotic rate of the PIM1 siRNA group was also higher than that of the NC and blank groups. In conclusion, our preliminary findings suggest that PIM1 gene silencing could inhibit proliferation and promote apoptosis of esophageal cancer cells.
Keywords: Esophageal cancer, PIM1, Eca109 cell line, proliferation, apoptosis, gene silencing
DOI: 10.3233/CBM-160038
Journal: Cancer Biomarkers, vol. 18, no. 2, pp. 149-154, 2017
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