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首页> 外文OA文献 >Honokiol inhibits gastric tumourigenesis by activation of 15-lipoxygenase-1 and consequent inhibition of peroxisome proliferator-activated receptor-gamma and COX-2-dependent signals
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Honokiol inhibits gastric tumourigenesis by activation of 15-lipoxygenase-1 and consequent inhibition of peroxisome proliferator-activated receptor-gamma and COX-2-dependent signals

机译：Honokiol inhibits gastric tumourigenesis by activation of 15-lipoxygenase-1 and consequent inhibition of peroxisome proliferator-activated receptor-gamma and COX-2-dependent signals

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Background and purpose: Peroxisome proliferator-activated receptor-gamma (PPAR-gamma), COX-2 and 15-lipoxygenase (LOX)-1 have been shown to be involved in tumour growth. However, the roles of PPAR-gamma, COX-2 or 15-LOX-1 in gastric tumourigenesis remain unclear. Here, we investigate the role of 15-LOX-1 induction by honokiol, a small-molecular weight natural product, in PPAR-gamma and COX-2 signalling during gastric tumourigenesis. Experimental approach: Human gastric cancer cell lines (AGS, MKN45, N87 and SCM-1) were cultured with or without honokiol. Gene and protein expressions were analysed by RT-PCR and Western blotting respectively. Small interfering RNAs (siRNAs) for COX-2, PPAR-gamma and 15-LOX-1 were used to interfere with the expressions of these genes. A xenograft gastric tumour model in mouse was used for in vivo study. Key results: PPAR-gamma and COX-2 proteins were highly expressed in gastric cancer cells. Inhibitors, or siRNA for COX-2 or PPAR-gamma, significantly decreased cell viability. Honokiol markedly inhibited PPAR-gamma and COX-2 expressions in gastric cancer cells and tumours of xenograft mice, and induced apoptosis and cell death. Honokiol markedly activated cellular 15-LOX-1 expression and 13-S-hydroxyoctadecadienoic acid (a primary product of 15-LOX-1 metabolism of linoleic acid) production. 15-LOX-1 siRNA could reverse the honokiol-induced down-regulation of PPAR-gamma and COX-2, and cell apoptosis. 15-LOX-1 was markedly induced in tumours of xenograft mice treated with honokiol. Conclusions and implications: These findings suggest that induction of 15-LOX-1-mediated down-regulation of a PPAR-gamma and COX-2 pathway by honokiol may be a promising therapeutic strategy for gastric cancer.
机译：背景和目的：已证明过氧化物酶体增殖物激活受体-γ（PPAR-γ），COX-2和15-脂氧合酶（LOX）-1与肿瘤的生长有关。然而，尚不清楚PPAR-γ，COX-2或15-LOX-1在胃肿瘤发生中的作用。在这里，我们调查小分子天然产物厚朴酚15-LOX-1诱导在胃肿瘤发生过程中PPAR-γ和COX-2信号传导中的作用。实验方法：在有或没有厚朴酚的情况下培养人胃癌细胞系（AGS，MKN45，N87和SCM-1）。通过RT-PCR和蛋白质印迹分别分析基因和蛋白质表达。使用COX-2，PPAR-γ和15-LOX-1的小干扰RNA（siRNA）来干扰这些基因的表达。小鼠体内异种移植胃肿瘤模型用于体内研究。关键结果：PPAR-γ和COX-2蛋白在胃癌细胞中高表达。 COX-2或PPAR-γ的抑制剂或siRNA会显着降低细胞活力。厚朴酚显着抑制胃癌细胞和异种移植小鼠肿瘤中PPAR-γ和COX-2的表达，并诱导细胞凋亡和细胞死亡。厚朴酚显着激活细胞15-LOX-1表达和13-S-羟基十八碳二烯酸（亚油酸15-LOX-1代谢的主要产物）的产生。 15-LOX-1 siRNA可以逆转厚朴酚诱导的PPAR-γ和COX-2的下调以及细胞凋亡。在厚朴酚处理的异种移植小鼠的肿瘤中明显诱导了15-LOX-1。结论和意义：这些发现表明，厚朴酚诱导15-LOX-1介导的PPAR-γ和COX-2通路下调可能是胃癌的一种有前途的治疗策略。

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