中文English
ISSN 1001-5256 (Print)
ISSN 2097-3497 (Online)
CN 22-1108/R
Volume 35 Issue 7
Jul.  2019
Turn off MathJax
Article Contents

Role of D-bifunctional protein in promoting the growth of hepatocellular carcinoma in rats and nude mice

DOI: 10.3969/j.issn.1001-5256.2019.07.022
Research funding:

 

  • Received Date: 2019-02-20
  • Published Date: 2019-07-20
  • Objective To investigate the expression of D-bifunctional protein ( DBP) in hepatocellular carcinoma ( HCC) tissue in rats and the growth of DBP-induced HCC in nude mice. Methods A total of 22 male Sprague-Dawley rats were randomly divided into normal control group with 8 rats and model group with 14 rats treated with intraperitoneally injected diethylnitrosamine to induce HCC, and Western blotting, immunohistochemistry, and RT-PCR were used to measure the expression of DBP. A total of 14 specific pathogen-free male BALB/c-nu mice were randomly divided into two groups. HepG2 cells were transfected with empty plasmid or DBP overexpression plasmid and were then injected subcutaneously into nude mice. There were 8 mice in the empty plasmid control group and 6 mice in the DBP high-expression plasmid group, and tumor size was measured for both groups. The t-test was used for comparison of continuous data between groups. Results The rats with HCC had significantly higher protein and mRNA expression of DBP in liver tissue than normal rats ( protein:1. 10 ± 0. 35 vs 0. 67 ± 0. 12, t =-7. 48, P < 0. 05; mRNA: 3. 70 ± 0. 85 vs 1. 17 ± 0. 72, t =-20. 46, P < 0. 05) . The DBP high-expression plasmid group had a significantly higher tumor volume than the empty plasmid group [ ( 7590. 50 ± 1867. 97) mm3 vs ( 1663. 78 ±420. 24) mm3, t =-39. 78, P < 0. 01]. Conclusion Highly expressed DBP can promote the progression of HCC in rats and thus provides a new target for the treatment of HCC and the research and development of inhibitory drugs.

     

  • loading
  • [1]LONG J, LIN J, WANG A, et al.PD-1/PD-L blockade in gastrointestinalcancers:Lessons learned and the road toward precision immunotherapy[J].J Hematol Oncol, 2017, 10 (1) :146.
    [2] SHIBATA M, MINAMI S, OE S, et al.Recognition of infection, status of outpatient treatment, and treatment history before carcinogenesis inpatients with viral hepatitis-associated liver cancer[J].Nihon Shokakibyo Gakkai Zasshi, 2016, 113 (10) :1734-1742.
    [3]CROAQH CM, LUBEL JS.Natural history of chronic hepatitis B:Phases in a complex relationship[J].World J Gastroenterol, 2014, 20 (30) :10395-10404.
    [4]MOELLER G, ADAMSKI J.Multifunctionality of human 17 betahydroxysteroid dehydrogenases[J].Mol Cell Endocrinol, 2006, 248 (1-2) :47-55.
    [5] ADAMSKI J, CARSTENSEN J, HUSEN B, et al.New 17 betahydroxysteroid dehydrogenases.Molecular and cell biology of the type IV porcine and human enzymes[J].Ann N Y Acad Sci, 1996, 784:124-136.
    [6]ZHA S, FERDINANDUSSE S, HICKS JL, et al.Peroxisomal branched chain fatty acid beta-oxidation pathway is upregulated in prostate cancer[J].Prostate, 2005, 63 (4) :316-323.
    [7]YE Z, YING YX, CHUAN BY, et al.Acetylation targets HSD17B4 for degradation via the CMA pathway in response to estrone[J].Autophagy, 2017, 13 (3) :538-553.
    [8]XIN L, PAN PM, YUN S, et al.NF-κB increased expression of 17β-hydroxysteroid dehydrogenase 4 promotes HepG2proliferation via inactivating estradiol[J].Mol Cell Endocrinol, 2015, 401:1-11.
    [9]MA PP.Inhibitory effects of vitamin K2 on HSD17B4-caused proliferation of human hepatocellular carcinoma cells and its mechanism[D].Shijiazhuang:Hebei Medical University, 2016. (in Chinese) 马盼盼.Vitamin K2抑制HSD17B4促肝癌细胞增殖的机制研究[D].石家庄:河北医科大学, 2016.
    [10]National Health and Family Planning Commission of the People’s Republic of China.Management, and treament of hepatocellular carcinoma (V2017) [J].J Clin Hepatol, 2017, 33 (8) :1419-1431. (in Chinese) .中华人民共和国国家卫生和计划生育委员会.原发性肝癌诊疗规范 (2017年版) [J].临床肝胆病杂志, 2017, 33 (8) :1419-1431.
    [11]ZHOU YL, LIU JY, YAO HW, et al.Increased expression of lncFOXC1 promotes liver cancer formation[J].Chin J Clin Pharmacol Ther, 2019, 24 (1) :27-31. (in Chinese) 周玉玲, 刘激扬, 姚红伟, 等.lncFOXC1表达增加促进肝癌发生[J].中国临床药理学与治疗学, 2019, 24 (1) :27-31.
    [12] XU X, YUAN GJ, DENG JJ, et al.Hepatic oval cells activated by hepatocyte apoptosis in diethylnitrosamine-induced rat liver cirrhosis[J].Saudi Med J, 2010, 31 (5) :490-494
    [13]BENSOUSSAN A, MYERS SP, WU SM, et al.Naturopathic and western hbrbal medicine practice in Australia-a workforce surey[J].Complement Ther Med, 2004, 12 (4) :17-27.
    [14]LIU RJ, YANG XZ, JIAO YT, et al.The animal model research of hepatic precancerous lesion induced by diethylnitrosamine[J].Chin J Integr Tradit West Med Liver Dis, 2015, 25 (3) :162-165. (in Chinese) 刘蕊洁, 杨先照, 焦云涛, 等.二乙基亚硝胺诱导肝细胞癌癌前病变动物模型研究[J].中西医结合肝病杂志, 2015, 25 (3) :162-165.
    [15]DE MS, KISSELENA T, FRANCIS H, et al.Liver carcinogenesis:Rodent models of hepatocarcinoma and cholangiocarcinoma[J].Dig Lver Dis, 2013, 45 (6) :450-459.
    [16] VELDHOVEN PP, CASTEELS M, MANNAERTS GP, et al.Further insights into peroxisomal lipid breakdown via alpha-an beta doxidation[J].Biochem Soc Trans, 2001, 29 (Pt2) :292-298.
    [17]LU X, KONG LY, LIU DQ, et al.Expression of D-bifunctional protein in hepatocellular carcinoma tissue and its correlation with alpha-fetoprotein and carbohydrate antigen 19-9 The animal model research of hepatic precancerous lesion induced by diethylnitrosamine[J].J Clin Hepatol, 2018, 34 (10) :2153-2156. (in Chinese) 路欣, 孔令玉, 刘殿卿, 等.D-双功能蛋白在肝癌组织中的表达及其与AFP和CA19-9的相关性[J].临床肝胆病杂志, 2018, 34 (10) :2153-2156.
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Article Metrics

    Article views (1306) PDF downloads(276) Cited by()
    Proportional views
    Related

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return