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目的:探讨胃癌细胞中β肾上腺能受体(β-ARs)与NF-κB通路及下游侵袭相关因子的关系。方法:分别用不同浓度普萘洛尔(10,30,100μmol/L)和异丙肾上腺素(50,100,200μmol/L)作用胃癌BGC-823和SGC-7901细胞株24 h后,用RT-PCR检测血管内皮生长因子(VEGF),环氧化酶2(COX-2),基质金属蛋白酶2(MMP-2),基质金属蛋白酶9(MMP-9)mRNA表达;用Western blot检测上述因子及NF-κB p65蛋白表达。结果:与对照细胞比较,普萘洛尔呈浓度依赖性降低两种胃癌细胞VEGF,COX-2,MMP-2,MMP-9的mRNA表达,而异丙肾上腺素则呈浓度依赖性升高上述因子的mRNA表达(均P<0.05);与对照组细胞比较,普萘洛尔作用后,两种胃癌细胞上述因子及NF-κB p65蛋白的表达明显下调,而异丙肾上腺素作用后则呈反向变化,且作用均呈浓度依赖性(均P<0.05)。结论:β-ARs与胃癌侵袭、转移密切相关,且其作用机制可能与增加NF-κB通路活性及其下游侵袭相关分子的表达有关。
Objective: To investigate the relationship between β adrenergic receptors (β-ARs) and NF-κB pathway and downstream invasive factors in gastric cancer cells. METHODS: Gastric cancer BGC-823 and SGC-7901 cell lines were treated with different concentrations of propranolol (10, 30, 100 μmol/L) and isoproterenol (50, 100, 200 μmol/L) for 24 h, and then detected by RT-PCR. Expression of endothelial growth factor (VEGF), cyclooxygenase-2 (COX-2), matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) mRNA; detection of these factors and NF-κB by Western blot P65 protein expression. Results: Compared with control cells, propranolol decreased the expression of VEGF, COX-2, MMP-2, and MMP-9 mRNA in two gastric cancer cells in a concentration-dependent manner, while isoproterenol showed a concentration-dependent increase. mRNA expression of factors (all P<0.05); Compared with control cells, the expression of these factors and NF-κB p65 protein were significantly down-regulated in propofolol and propionolol, but after isoproterenol action The changes were reversed and the effects were concentration-dependent (all P<0.05). Conclusion: β-ARs is closely related to the invasion and metastasis of gastric cancer, and its mechanism may be related to the increase of NF-κB pathway activity and the expression of downstream invasive molecules.