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首页> 外文期刊>RSC Advances >Celastrol delays hepatic steatosis and carcinogenesis in a rapid AKT/c-Met-transfected hepatocellular carcinoma model via suppressing fatty acid synthase expression and AKT/ERK phosphorylation
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Celastrol delays hepatic steatosis and carcinogenesis in a rapid AKT/c-Met-transfected hepatocellular carcinoma model via suppressing fatty acid synthase expression and AKT/ERK phosphorylation

机译：Celastrol通过抑制脂肪酸合成酶表达和AKT / ERK磷酸化，延迟肝脏脂肪变性和致癌作用。通过抑制脂肪酸合成酶表达和AKT / ERK磷酸化，促进Akt / C-Met转染的肝细胞癌模型

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摘要

Although the suppressing effects of celastrol on hepatocellular carcinoma (HCC) have been demonstrated, evidence for the targeting of fatty acid synthetase (FASN) in the development of HCC by celastrol is still rare. In this study, the effect of celastrol on a rapid HCC model featuring co-activation of AKT/c-Met oncogenes in mice was studied. The effect of celastrol on the alpha-fetoprotein level in the liver and serum was also investigated. Protein expressions of PCNA, Ki67 and FASN in celastrol-treated AKT/c-Met HCC mice were observed. The molecular mechanism of celastrol on the AKT/c-Met signaling pathway was elucidated. The results revealed that celastrol significantly repressed the AKT/c-Met induced HCC development and down-regulated the mRNA expression of AFP in the liver and the AFP level in serum. Furthermore, the expression of proliferation-associated proteins in the HCC tissues was reduced by celastrol treatment. Moreover, the abundant steatosis that resulted from FASN accumulation in the liver in AKT/c-Met mice was also attenuated. Finally, the phosphorylation of AKT and ERK1/2 in HCC mice was repressed by celastrol treatment. Overall, our data demonstrate that celastrol exerts an antiproliferative and novel lipid-decreasing effect by targeting AKT/ERK and FASN in HCC development in vivo.
机译：虽然已经证明了Celastrol对肝细胞癌（HCC）对肝细胞癌（HCC）的抑制作用，但Celastrol在HCC开发中靶向脂肪酸合成酶（FASN）的证据仍然很少见。在这项研究中，研究了Celastrol对特征在小鼠中Akt / C-Met oncocogenes的共激活的快速HCC模型的影响。还研究了Celastrol对肝脏和血清中α-胎儿蛋白水平的影响。观察到在Celastrol治疗的AKT / C-Met HCC小鼠中PCNA，KI67和FASN的PCNA，KI67和FASN的蛋白表达。阐明了Celastrol对AKT / C-Met信令途径的分子机制。结果表明，Celastrol显着压抑了AKT / C-MET诱导的HCC开发，下调了肝脏中AFP的mRNA表达和血清中的AFP水平。此外，通过Celastrol治疗减少了HCC组织中增殖相关蛋白的表达。此外，Akt / C-Met小鼠中来自肝脏的FasN积累的丰富脂肪也是衰减的。最后，通过Celastrol治疗压抑了HCC小鼠中Akt和Erk1 / 2的磷酸化。总体而言，我们的数据表明Celastrol通过靶向Akt / Erk和Fasn在体内HCC开发中施用抗增殖和新的脂质降低效果。

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  • 来源
    《RSC Advances》 |2018年第25期|共8页
  • 作者

    Hu Junjie; Li Xin; Zhou Junxuan; Zhang Cong; Zheng Guohua; Qiu Zhenpeng;

  • 作者单位

    Hubei Univ Chinese Med Coll Pharm 1 West Huangjiahu Rd Wuhan 430065 Hubei Peoples R China;

    Hubei Univ Chinese Med Coll Pharm 1 West Huangjiahu Rd Wuhan 430065 Hubei Peoples R China;

    Hubei Univ Chinese Med Coll Pharm 1 West Huangjiahu Rd Wuhan 430065 Hubei Peoples R China;

    Hubei Univ Chinese Med Coll Pharm 1 West Huangjiahu Rd Wuhan 430065 Hubei Peoples R China;

    Hubei Univ Chinese Med Key Lab Chinese Med Resource &

    Compound Prescript Minist Educ 1 West Huangjiahu Rd Wuhan 430065 Hubei Peoples R China;

    Hubei Univ Chinese Med Coll Pharm 1 West Huangjiahu Rd Wuhan 430065 Hubei Peoples R China;

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  • 正文语种 eng
  • 中图分类 化学;
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