HBx过表达对肝癌HepG2细胞AKT、PI3K表达的影响
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摘要
目的研究乙型肝炎病毒X蛋白(HBx)对肝癌细胞增殖的影响,并探索HBx过表达对肝癌细胞PI3K/AKT表达的影响。方法构建过表达HBx的肝癌HepG2细胞,测定其荧光素酶的表达,采用MTT法研究肝癌细胞增殖情况,采用Western blotting法对各组细胞PI3K及AKT的表达情况进行研究。结果成功构建了过表达HBx的肝癌HepG2细胞,HBx有促进肝癌细胞增殖的作用,进一步研究发现,过表达HBx有上调肝癌细胞PI3K及AKT表达的作用。结论 HBx有促进肝癌细胞增殖作用,其机制可能与上调PI3K/AKT表达有关。
Objective To study the effect of HBx on the proliferation of hepatocellular carcinoma cells,and to explore its relationship with PI3 K/AKT. Methods Overexpression of HBx in HepG2 cells was constructed and their luciferase expression was determined. MTT method was used to study the proliferation of hepatocellular carcinoma cells.Western blotting was used to study the expressions of PI3 K and AKT in each group. Results The overexpression of HBx in HepG2 cells was constructed successfully,which promoted the proliferation of hepatocellular carcinoma cells.Further studies showed that overexpression of HBx could up-regulate the expressions of PI3 K and AKT. Conclusion HBx has the effect of promoting the proliferation of hepatocellular carcinoma cells,and its mechanism may be related to the up-regulation of PI3 K/AKT expression.
Objective To study the effect of HBx on the proliferation of hepatocellular carcinoma cells,and to explore its relationship with PI3 K/AKT. Methods Overexpression of HBx in HepG2 cells was constructed and their luciferase expression was determined. MTT method was used to study the proliferation of hepatocellular carcinoma cells.Western blotting was used to study the expressions of PI3 K and AKT in each group. Results The overexpression of HBx in HepG2 cells was constructed successfully,which promoted the proliferation of hepatocellular carcinoma cells.Further studies showed that overexpression of HBx could up-regulate the expressions of PI3 K and AKT. Conclusion HBx has the effect of promoting the proliferation of hepatocellular carcinoma cells,and its mechanism may be related to the up-regulation of PI3 K/AKT expression.
引文
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[15] JUNG K H,RUMMAN M,YAN H,et al. An ethylacetate fraction of Ar-temisia capillaris(ACE-63)induced apoptosis and anti-angiogenesis viainhibition of PI3K/AKT signaling in hepatocellular carcinoma[J].Phytother Res,2018,32(10):2034-2046. DOI:10. 1002/ptr. 6135.
[2] JEMAL A,BRAY F,CENTER M M,et al. Global cancer statistics[J].CA Cancer J Clin,2011,61(2):69-90. DOI:10. 3322/caac. 20107.
[3] CHEN W,ZHENG R,ZENG H,et al. Annual report on status ofcancer in China,2011[J]. Chin J Cancer Res,2015,27(1):2-12.DOI:10. 3978/j. issn. 1000-9604. 2015. 01. 06.
[4]王福成,元刚,孙咏红,等.泛素特异性肽酶22对肝癌细胞凋亡的影响及机制研究[J].胃肠病学和肝病学杂志,2018,27(6):629-634. DOI:10. 3969/j. issn. 1006-5709. 2018. 06. 007.WANG F C,YUAN G,SUN Y H,et al. Effect of USP22 on apoptosisof hepatocellular carcinoma cells and its mechanism[J]. Chin JGastroenterol Hepatol,2018,27(6):629-634. DOI:10. 3969/j.issn. 1006-5709. 2018. 06. 007.
[5] KUDO M. m TOR inhibitor for the treatment of hepatocellular carcinoma[J].Dig Dis,2011,29(3):310-315. DOI:10. 1159/000327565.
[6] JUNG K H,CHOI M J,HONG S,et al. HS-116,a novel phosphati-dylinositol 3-kinase inhibitor induces apoptosis and suppresses angio-genesis of hepatocellular carcinoma through inhibition of the PI3K/AKT/m TOR pathway[J]. Cancer Lett,2012,316(2):187-195.DOI:10. 1016/j. canlet. 2011. 10. 037.
[7] BOUCHARD M J,SCHNEIDER R J. The enigmatic X gene of hepati-tis B virus[J]. J Virol,2004,78(23):12725-12734. DOI:10.1128/JVI. 78. 23. 12725-12734. 2004.
[8] WANG F Z,FEI H R,LIAN L H,et al. Hepatitis B x-interacting pro-tein induces Hep G2 cell proliferation through activation of the phos-phatidylinositol 3-kinase/AKT pathway[J]. Exp Biol Med(May-wood),2011,236(1):62-69. DOI:10. 1258/ebm. 2010. 010179.
[9] LIU H,XU L,HE H,et al. Hepatitis B virus X protein promotes hepa-toma cell invasion and metastasis by stabilizing Snail protein[J]. CancerSci,2012,103(12):2072-2081. DOI:10. 1111/cas. 12017.
[10] YU J S,CUI W. Proliferation,survival and metabolism:the role of PI3K/AKT/m TOR signaling in pluripotency and cell fate determination[J].Development, 2016, 143(17):3050-3060. DOI:10. 1242/dev. 137075.
[11] NOZHAT Z,HEDAYATI M. PI3K/AKT pathway and its mediators inthyroid carcinomas[J]. Mol Diagn Ther,2016,20(1):13-26.DOI:10. 1007/s40291-015-0175-y.
[12] YANG S X,POLLEY E,LIPKOWITZ S. New insights on PI3K/AKTpathway alterations and clinical outcomes in breast cancer[J]. CancerTreat Rev,2016,(45):87-96. DOI:10. 1016/j. ctrv. 2016. 03. 004.
[13]夏天放,徐果.中性粒细胞弹性蛋白酶对HepG2细胞增殖的影响及其机制的研究[J].胃肠病学和肝病学杂志,2016,25(9):1009-1013. DOI:10. 3969/j. issn. 1006-5709. 2018. 06. 007.XIA T F,XU G. The mechanism and effect of neutrophil elastase on pro-liferation of Hep G2 cells[J]. Chin J Gastroenterol Hepatol,2016,25(9):1009-1013. DOI:10.3969/j. issn.1006-5709.2018.06.007.
[14] SADEK K M,LEBDA M A,NASR N E,et al. Role of lncRNAs asprognostic markers of hepatic cancer and potential therapeutic targe-ting by S-adenosylmethionine via inhibiting PI3K/Akt signaling path-ways[J]. Environ Sci Pollut Res Int,2018,25(20):20057-20070. DOI:10. 1007/s11356-018-2179-8.
[15] JUNG K H,RUMMAN M,YAN H,et al. An ethylacetate fraction of Ar-temisia capillaris(ACE-63)induced apoptosis and anti-angiogenesis viainhibition of PI3K/AKT signaling in hepatocellular carcinoma[J].Phytother Res,2018,32(10):2034-2046. DOI:10. 1002/ptr. 6135.