RESUMO
Objective: To explore the effects of HIF-1α (hypoxia-inducible factor-1α), β-catenin, IMP3 (insulin-like growth factor II mRNA-binding protein 3) and PCNA (proliferating cell nuclear antigen) on proliferation of gastric cancer SGC-7901 cells. Methods: The pcDNA™ 6.2-GW/EmGFP-miR- β-catenin plasmid was transfected into SGC-7901 cells to establish stably transfected cell line miR- β-catenin-7901. In this experiment, four groups were designed: control group (SGC-7901 cells were cultured under normoxic conditions), hypoxia group (SGC-7901 cells were cultured under hypoxic conditions), transfection group (miR-β-catenin-7901 cells were cultured under normoxic conditions), and combination of transfection and hypoxia group (miR-β-catenin-7901 cells were cultured under hypoxic conditions). The proliferation of SGC-7901 cells in four groups was detected by colony formation assay and cell doubling time assay. The expression levels of HIF-1α, β-catenin, IMP3 and PCNA proteins of SGC-7901 cells in four groups were detected by Western blotting. Results: As compared with the control group, the number of colonies was increased and the cell doubling time was shortened in hypoxia group (P < 0.05). As compared with the hypoxia group, the number of colonies was reduced and the cell doubling time was prolonged in the combination of transfection and hypoxia group (P < 0.05). The expression levels of HIF-1α, β-catenin, IMP3 and PCNA proteins in hypoxia group were higher than those in the control group (P < 0.05). The expression levels of HIF-1α, β-catenin, IMP3 and PCNA proteins in the transfection group were lower than those in the control group (P < 0.05). The expression levels of HIF-1α, β-catenin, IMP3 and PCNA proteins in the combination of transfection and hypoxia group were lower than those in the hypoxia group (P < 0.05). Conclusion: The proliferation of gastric cancer SGC-7901 cells may be related to the interaction of HIF-1α and β-catenin, which resulted in the increased expression levels of IMP3 and PCNA. Copyright © 2013 by TUMOR.