期刊文献+

冈田酸对喉鳞癌细胞系PP2A活性及迁移的影响 被引量:1

Okadaic acid inhibits PP2A activities and cell migration of laryngeal squamous cell carcinoma Hep-2
下载PDF
导出
摘要 目的:探讨冈田酸(OA)对喉鳞癌细胞系(Hep-2)活性和迁移能力的影响及其可能的作用机制。方法:采用四甲基噻唑蓝(MTT)比色实验确定OA作用于Hep-2的最大浓度;酶活性实验检测不同浓度(0、50、100 n mol/L)OA对Hep-2蛋白磷酸酶2A(PP2A)活性的影响;划痕实验检测Hep-2在不同浓度(0、50、100 nmol/L)OA作用下迁移能力的变化。结果:50、100、200 nmol/L OA作用24 h后Hep-2的相对活力分别为96.7%±1.8%、82.9%±12.6%和57.2%±7.7%,与对照组(100%)比较均明显下降(P均<0.05)。50和100 nmol/L OA作用24 h后PP2A的相对活性分别为30.90%±12.01%和8.98%±4.96%,与对照组(100%)相比明显下降(P<0.05)。划痕试验中,经OA作用24及48 h后Hep-2细胞的迁移能力与对照组相比均明显减弱(P<0.05),并且100 nmol/L OA处理组迁移能力的减弱程度较50nmol/L OA处理组更明显(P<0.05)。结论:100 n mol/L冈田酸明显抑制Hep-2细胞PP2A活性并降低了细胞的迁移能力。 OBJECTIVE:To investigate the mechanism of inhibition of Hep-2 cell migration by Okadaic acid(OA). METHODS:MTT assay was used to determine the doses of OA for the investigation. Hep-2 cells were treatedwith 0,50 or 100 nmol/L OA and enzyme assay was used to measure PP2A activities. Wound scratch assay was used toobserve the influence of OA on migration of Hep-2. RESULTS:The growth inhibition ratio was 96.7%±1.8%,82.9%± 12.6% and 57.2%±7.7% in cells treated with 50,100 and 200 nmol/L OA,and the difference wassignificant (P〈0.05). In cells treated with 50 and 100 nmol/L OA,the relative activity of PP2A was 30.90%±12.01% and8.98%±4.96% (P〈 0.05). From the wound scratch assay,the treated cells took significantly longer than untreated cells forhealing (P〈0.05). CONCLUSION:Inhibition of PP2A activities may be responsible for the reduction of migration in theOA-treated Hep-2 cells.
出处 《癌变.畸变.突变》 CAS CSCD 2016年第4期273-276,280,共5页 Carcinogenesis,Teratogenesis & Mutagenesis
基金 浙江省自然科学基金(LY13H130001) 浙江省科技厅项目(2013 C33208) 浙江省中医药管理局项目(2012ZA085)
关键词 冈田酸 HEP-2细胞系 喉鳞状细胞癌 蛋白磷酸酶2A 迁移 Okadaic acid Hep-2 laryngeal squamous cell carcinoma protein phosphatase 2A migration
  • 相关文献

参考文献1

二级参考文献14

  • 1Eichhorn PJ, Creyghton MP, Bernards R. Protein phosphatase 2A regulatory subunits and cancer[J]. Biochim Biophys Acta, 2009, 1795(1): 1-15.
  • 2Li HH, Cai X, Shouse GP, et al. A specific PP2A regulatory subunit, B56gamma, mediates DNA damage-induced dephos- phorylation of p53 at Thr55[J]. EMBO J, 2007, 26 (2) : 402- 411.
  • 3Shouse GP, Cai X, Liu X. Serine 15 phosphorylation of p53 directs its interaction with B56gamma and the tumor suppressor activity of B56gamma-specific protein phosphatase 2A[J]. Mol CellBiol, 2008, 28 (1): 448-456.
  • 4Shouse GP, Nobumori Y, Liu X. A B56gamma mutation in lung cancer disrupts the p53-dependent tumor-suppressor function of protein phosphatase 2A[J]. Oncogene, 2010, 29 (27): 3933-3941.
  • 5Chen W, Possemato R, Campbell KT, et al. Identification of specific PP2A complexes involved in human cell transformation [J]. CaneerCell, 2004, 5 (2): 127-136.
  • 6Haase H, Ober-B15baum JL, Engelhardt G, et al. Cadmium ions induce monoeytic production of tumor necrosis factor-alpha by inhibiting mitogen activated protein kinase dephosphorylation [J].Toxicol Lett, 2010, 198 (2): 152-158.
  • 7Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation[J]. Cell, 2011, 144 (5): 646-674.
  • 8Chen L, Liu L, Huang S. Cadmium activates the mitogen- activated protein kinase (MAPK) pathway via induction of reactive oxygen species and inhibition of protein phosphatases 2A and 5[J]. Free Radie Biol Med, 2008, 45 (7): 1035-1044.
  • 9Stohs SJ, Bagchi D, Hassoun E, et al. Oxidative mechanisms in the toxicity of chromium and cadmium ions[J]. J Environ PatholToxicolOneol, 2001, 20(2): 77-88.
  • 10Alison MR, Nicholson LJ, Lin WR. Chronic inflammation andhepatocellular carcinoma[J]. Recent Results Cancer Res, 2011, 185: 135-148.

共引文献2

同被引文献6

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部