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首页> 外文期刊>RSC Advances >Celecoxib attenuates hepatocellular proliferative capacity during hepatocarcinogenesis by modulating a PTEN/NF-κB/PRL-3 pathway
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Celecoxib attenuates hepatocellular proliferative capacity during hepatocarcinogenesis by modulating a PTEN/NF-κB/PRL-3 pathway

机译：Celecoxib通过调节PTEN / NF-κB/ PRL-3途径，在肝癌发生过程中衰减肝细胞增殖能力

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摘要

Although the efficacy of celecoxib on various cancer cell behaviors, including aberrant proliferation, in cultured hepatocellular carcinoma (HCC) cells has been demonstrated, whether celecoxib regulates cell proliferation by targeting PRL-3-associated signaling transduction during hepatocarcinogenesis in vivo has been incompletely studied. Here, we investigate the anti-proliferative efficacy of celecoxib in a rapid HCC mouse model established by hydrodynamic transfection of activated AKT and c-Met proto-oncogenes. The results show that celecoxib is effective at delaying the malignant transformation of hepatocytes by reducing the protein expression of Ki67, Cyclin D1 and c-Myc in the AKT/c-Met HCC-bearing mice. Mechanistically, celecoxib increases the protein expression of PTEN and suppresses the protein expression of NF-κB and PRL-3 in the liver of the HCC mice. Using PTEN-silenced and LPS-stimulated approaches in vitro , a mechanism by which celecoxib regulates a PTEN/NF-κB/PRL-3 pathway in HCC cells was illuminated. Altogether, our study demonstrates that celecoxib attenuates the hepatocellular proliferative capacity during hepatocarcinogenesis, which is probably attributable to its regulation of the PTEN/NF-κB/PRL-3 pathway.
机译：尽管已经证明了Celecoxib对各种癌细胞行为（包括异常增殖）的疗效，包括在培养的肝细胞癌（HCC）细胞中，Celecoxib是否通过针对体内肝癌发生期间靶向PRL-3相关的信号转导的细胞增殖已经不完全研究。在此，我们研究Celecoxib在由活性AKT和C-MET原型癌基因的流体动力转染的快速HCC小鼠模型中的抗增殖效果。结果表明，Celecoxib通过减少KI67，Cyclin D1和C-Myc的蛋白质表达延迟肝细胞的恶性转化，在AKT / C-Met HCC轴承小鼠中减少。机械地，Celecoxib增加了PTEN的蛋白质表达，并在HCC小鼠的肝脏中抑制NF-κB和PRL-3的蛋白质表达。在体外使用PTEN沉默和LPS刺激的方法，通过其中Celecoxib调节HCC细胞中PTEN / NF-κB/ PRL-3途径的机制。完全，我们的研究表明，Celecoxib在肝癌发生期间衰减肝细胞增殖能力，这可能涉及其对PTEN / NF-κB/ PRL-3途径的调节。

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