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Plk1、Chk1/2在原发性肝癌组织及HepG2细胞中的表达研究 被引量:6

Expression and significance of Plk1,Chk1/2 protein in primary hepatic carcinoma tissue and HepG2 cell
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摘要 目的:研究保罗样激酶1(Polo-like kinase1,Plk1)、细胞周期检测点激酶1、2(Checkpoint kinase 1/2,Chk1/2)在原发性肝癌组织与人肝癌细胞Hep G2中的表达情况。方法:使用免疫组织化学Envision法检测40例原发性肝癌组织及16例肝非肿瘤组织中Plk1、Chk1/2蛋白的表达。提取培养后的Hep G2细胞蛋白。利用蛋白免疫印记(Western blot)技术定性分析Plk1、Chk1/2蛋白在Hep G2细胞中的表达情况,并测定灰度值进行定量分析。结果:原发性肝癌组织中Plk1、Chk1蛋白的阳性表达率分别是57.5%、75%,高于它们在肝非瘤组织中的表达率0%、25.0%(P<0.05)。Chk2在原发性肝癌组织中的表达阳性率22.5%,低于肝非肿瘤组织中的表达率56.3%(P<0.05)。Plk1、Chk1/2蛋白在Hep G2细胞中均有表达。其相对表达量分别是:0.39±0.022 6、0.08±0.024 9、0.01±0.006 6,三者之间的差异均有统计学意义,其表达的顺序依次为Plk1>Chk1>Chk2。结论:Plk1、Chk1蛋白在原发性肝癌组织中表达上调,而Chk2蛋白在原发性肝癌组织中表达下调。Plk1、Chk1/2基因作为细胞周期调控中的重要激酶在Hep G2细胞中均有表达,其表达顺序为Plk1>Chk1>Chk2。Plk1、Chk1具有相对意义的肿瘤选择性表达,可能成为肝癌生物治疗中新的治疗靶点。 Objective: To investigate the expression of Plk1( Polo-like kinase 1) and Chk1 /2( Checkpoint kinase 1 /2) in primary hepatic carcinoma tissue and Hep G2 cell. Methods: Using immunohistochemistry chemical method detected expression of Plk1,Chk1 /2 protein in 40 cases of primary hepatic carcinoma tissue and 16 cases of non-tumor tissue of liver. Western blot was applied to detect the expression of Plk1 and Chk1 /2 protein in HepG2 cells,and gray value was measured by using the quantitative analysis. Results: The positive rate of Plk1,Chk1 /2 protein expression in primary hepatic carcinoma was 57. 5%,75. 0% and 22. 5%respectively,compared with positive rate in the liver of non-tumor tissue were 0%,25. 0% and 56. 3%. The expression of Plk1 and Chk1 protein in primary hepatic carcinoma tissue is higher than that in non-tumor tissue of liver,and the difference was statistically significant( P〈0. 05). The expression of Chk2 in primary hepatic carcinoma was lower than that in hepatic non-tumor tissue,and the difference was statistically significant( P〈0. 05) too. The expression of Plk1,Chk1 /2 protein were detected in HepG2 cells and the relative expression rate of Plk1,Chk1 /2 protein were 0. 39 ± 0. 0226,0. 08 ± 0. 0249 and 0. 01 ± 0. 0066 respectively,the difference between them was statistically significant. The expression degree was Plk1 Chk1 Chk2. Conclusion: Plk1,Chk1 protein in primary hepatic carcinoma was up-regulated,while Chk2 protein was down-regulated in these tissues. The expression degree was Plk1 Chk1 Chk2. There were relatively selective expression in primary hepatic carcinoma tissue of Plk1,Chk1 protein,then Plk1 and Chk1 might be ideal targets for therapy of primary hepatic carcinoma.
出处 《中国免疫学杂志》 CAS CSCD 北大核心 2015年第6期758-760,763,共4页 Chinese Journal of Immunology
基金 贵州省科技厅科学技术基金资助项目([2008]2170号)
关键词 PLK1 CHK1/2 HEPG2 原发性肝癌 Plk1 Chk1/2 HepG2 cell Primary hepatic carcinoma
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  • 1安立峰,董震.RNA干扰——肿瘤研究的新工具[J].中华肿瘤杂志,2005,27(7):385-388. 被引量:38
  • 2Xue-Hua Chen,Bin Lan,Ying Qu,xiao-Qing Zhang,Qu Cai,Bing-Ya Liu,Zheng-Gang Zhu.Inhibitory effect of Polo-like kinase 1 depletion on mitosis and apoptosis of gastric cancer cells[J].World Journal of Gastroenterology,2006,12(1):29-35. 被引量:10
  • 3Hirose Y, Berger MS, Pieper RO. Abrogation of the Chk1-mediat ed G(2) checkpoint pathway potentiates temozolomide-induced tox icity in a p53-independent manner in human glioblastoma cells. Cancer Res, 2001 ; 61:5843 - 5849
  • 4Melo J, Toczyski D. A unified view of the DNA-damage check point. Curr Opin Cell Biol, 2002; 14:237- 245
  • 5Walworth NC, DNA damage: Chk1 and Cdc25, more than meets the eye. Curr Opin Genet Dev, 2001; 11:78- 82
  • 6Bartek J, Falck J, Lukas J, Chk2 kinase- a busy messenger. Nat Rev Mol Cell Biol, 2001 ;2:877 - 886
  • 7Pawlik TM, Keyomarsi K. Role of cell cycle in mediating sensitivity to radiotherapy, lnt J Radiat Oncol Biol Phys, 2004, 59 : 928-942.
  • 8Raju U, Nakata E, Yang P, et al. In vitro enhancement of tumor cell radiosensitivity by a selective inhibitor of cyclooxygenase-2 enzyme: mechanistic considerations. Int J Radiat Oncol Biol Phys,2002, 54:886-894.
  • 9Theron T, Binder A, Verheye-Dua F, et al. The role of G2-block abrogation, DNA double-strand break repair and apoptosis in the radiosensitization of melanoma and squamous squamous cell carcinoma cell lines by pentoxifylline. Int J Radiat Biol, 2000, 76:1197-1208.
  • 10Zhou BB, Chaturvedi P, Spring K, et al. Caffeine abolishes the mammalian G2/M DNA damage checkpoint by inhibiting ataxiatelangiectasia-mutated kinase activity. J Biol Chem, 2000, 275:10342-10348.

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