USP18 Promotes Apoptosis of Liver Cancer Cells Induced by NDV

被引：0
|
作者：
Zhu H. [1 ,2 ,3 ]
Chen J. [1 ,2 ,3 ]
Xu Y. [1 ,2 ,3 ]
Xue B. [1 ,2 ,3 ]
Wang X. [1 ,2 ,3 ]
Deng R. [1 ,2 ,3 ]
Tian R. [1 ,2 ,3 ]
Chen S. [1 ,2 ,3 ]
Wang J. [1 ,2 ,3 ]
Huang X. [1 ,2 ,3 ]
机构：
[1] College of Biology, Hunan University, Changsha
[2] Institute of Pathogen Biology and Immunology, Hunan University, Changsha
[3] State Key Laboratory of Chemo/Biosensing and Chemometrics, Hunan University, Changsha
来源：
Hunan Daxue Xuebao/Journal of Hunan University Natural Sciences | 2019年 / 46卷 / 06期
基金：
中国国家自然科学基金;
关键词：
Bax; Cell apoptosis; ISG12a; Liver cancer cell; Mitochondria; NDV; NOXA; USP18;
D O I：
10.16339/j.cnki.hdxbzkb.2019.06.013
中图分类号：
学科分类号：
摘要：
After NDV infects the liver tumour cell, USP18 (Ubiquitin Specific Protease 18) acts as a deubiquitin enzyme and cleaves ubiquitin from ubiquitinated protein substrates. NDV infection of liver tumour cell can induce the apoptosis of cancer cells. Infection with NDV up-regulates the expression of USP18, and the role of USP18 in the apoptosis induced by NDV was investigated. In this study, the liver tumour cell line Huh7 is taken as the system, and western blot and qualitative PCR are considered. It is found that USP18 promotes the apoptosis of cancer cells induced by NDV, which demonstrates that USP18 has the anticancer function. In contrast, knock-down of USP18 inhibits the apoptosis of the cancer cells, which reveals that USP18 can positively regulate the protein level of Bax and NOXA. Consistently, overexpression of USP18 enhances the permeability of mitochondrial membrane and promotes the release of CYTOCHROME C. Similarly, overexpression of USP18 increases the cleaved caspase-7 and strengthens the apoptosis as well. It is also found that USP18 can upregulate the protein level of ISG12a(IFN-stimulated gene 12a). It attenuates the ubiquitination degradation of ISG12a. The findings in this research provide a profound influence and a new insight towards treatment for liver cancer. © 2019, Editorial Department of Journal of Hunan University. All right reserved.
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页码：88 / 95
页数：7
相关论文
共 34 条
  • [1] Kim J., Sinn D.H., Choi M.S., Et al., Hepatocellular carcinoma with extrahepatic metastasis: are there still candidates for transarterial chemoembolization as an initial treatment, PLOS One, 14, 3, (2019)
  • [2] Takaki A., Kawano S., Uchida D., Et al., Paradoxical roles of oxidative stress response in the digestive system before and after Carcinogenesis, Cancers, 11, 2, pp. 213-219, (2019)
  • [3] Mu D., Yuan F.C., Chen Y., Et al., Baseline value of intrahepatic HBV DNA over cccDNA predicts patient's response to interferon therapy, Scientific Reports, 7, 1, pp. 5937-5943, (2017)
  • [4] Allweiss L., Dandri M., The role of cccDNA in HBV maintenance, Viruses, 156, 9, pp. 1-12, (2017)
  • [5] Chong C.K., Cheng C.Y.S., Tsoi S.Y.J., Et al., Role of hepatitis B core protein in HBV transcription and recruitment of histone acetyltransferases to cccDNA minichromosome, Antiviral Research, 144, pp. 1-7, (2017)
  • [6] Vanwolleghem T., Boonstra A., Focus on the liver: host-virus interactions in HBV, Journal of Hepatology, 66, 5, pp. 884-885, (2017)
  • [7] Kinoshita W., Ogura N., Watashi K., Et al., Host factor PRPF31 is involved in cccDNA production in HBV-replicating cells, Biochemical and Biophysical Research Communications, 482, 4, pp. 638-644, (2017)
  • [8] Assuncao S.N.F., Sorte N.C.B., Alves C.D., Et al., Nonalcoholic fatty liver disease (NAFLD) pathophysiology in obese children and adolescents: update, Nutricion Hospitalaria, 34, 3, pp. 727-730, (2017)
  • [9] Ballestri S., Nascimbeni F., Baldelli E., Et al., NAFLD as a sexual dimorphic disease: role of gender and reproductive status in the development and progression of nonalcoholic fatty liver disease and inherent cardiovascular risk, Advances in Therapy, 34, 6, pp. 1291-1326, (2017)
  • [10] An X., Yang Z., An Z., MiR-149 compromises the reactions of liver cells to fatty acid via its polymorphism and increases non-alcoholic fatty liver disease (NAFLD) risk by targeting methylene tetrahydrofolate reductase (MTHFR), Medical Science Monitor: International Medical Journal of Experimental and Clinical Research, 23, pp. 2299-2307, (2017)
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