| Objective：To investigate the influence of silencingnuclear factor-κB (NF-κB) on the proliferation and invasion ofgastric cancer SGC-7901cells exposed to hypoxia and itspossible mechanism.Methods: SGC-7901cells were transfected with plasmidpcDNA6.2-GW/EmGFPmiR-NF-κB, from which stably transfected cellline SGC-7901was screened. Four groups were set up and they were controlgroup, hypoxia group, transfection group and combined group oftransfection and hypoxia. Colony-formation assay, cell doubling time assay,the volume, weight and growth curve of transplantation tumor were used totest the proliferation of four groups after different intervening measure. Thecell viability were detected with Typan blue test. The expressions of NF-κB,HIF-1α and PLD-1at protein levels were analyzed byimmunohistochemistry and Western blot.Results: Proliferation: Compared with control group, the proliferation capacity of hypoxia group was increased but the transfection group andcombined group were decreased(P＜0.05). Cell viability: Compared withcontrol group, the cell viability of transfection group and combined groupwere decreased(P＜0.05), however, there was no obvious change in thehypoxia group. Invasion: Compared with control group, the invasioncapacity of hypoxia group was markedly increased but the transfectiongroup and combined group were decreased(P＜0.05). Protein localization:NF-κB protein was expressed both in the nucleus and cytoplasm underhypoxia condition, and given priority to the former. Protein expressionlevel: Compared with control group, the expressions of NF-κB, HIF-1αandPLD-1in transfection group were suppressed while the hypoxia group wereup-regulated (P＜0.05). Compared with hypoxia group, those three proteinsin combined group were decreased (P＜0.05).Conclusion: HIF-1α and NF-κB may have interrelationship inhypoxia condition and suppression of NF-κB can induce proliferation andinvasion inhibition of hypoxia gastric cancer cells via HIF-1α and PLD-1restraining. |
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