ABSTRACT
Objective To determine the effect of signal transducers and activators of transcription 3 (STAT3) gene silencing by shRNA mediated by lentiviral vector for the treatment of colorectal cancer. Methods The recombinant lentiviral vector pRNAT-shSTAT3, empty lentiviral vector pRNAT-GFP, and lentiviral packaging plasmids in supernatant were collected to transfect HT-29 cells for harvesting the HT-29-shSTAT3 cells and HT29-GFP cells. Fifteen male rats were divided into three groups (n = 5 ), and then they were inoculated with HT-29cells, HT-29-GFP cells and HT-29-shSTAT3 cells, respectively. Cell growth was assessed by MTT assay and the changes in cell cycle were detected by flow cytometry. The changes in microvessel density (MVD) of tumors were detected by immunohistochemistry. All data were analysed by one-way analysis of variance. Results The growth of HT-29-shSTAT3 cells was significantly suppressed compared with HT-29 and HT-29-GFP cells (F = 632.50,P ＜ 0. 05 ). The proportions of cells at the G0/G1 phase were 68.7% ± 2.9% in HT-29-shSTAT3 cells, 38.5% ±1.6% in HT-29-GFP cells and 38.7% ± 2.3% in HT-29 cells, with a significant difference among the three groups (F = 166.53, P ＜ 0.05 ). The MVDs of HT-29 cells, HT-29-GFP cells and HT-29-shSTAT3 cells were 29 ±5, 28 ±4 and 10 ±3, respectively, with a significant difference among the three groups (F=31.60, P ＜0.05). Conclusion STAT3 gene silencing by shRNA mediated by lentiviral vector can significantly inhibit the growth of colorectal cancer cells.