期刊文献+

肺癌中P-AKT的表达与血管生成 被引量:6

Relationship between expression of P-AKT and angiogenesis of non-small cell lung cancer
暂未订购
导出
摘要 目的:探讨磷酸化蛋白激酶B(P-AKT)在非小细胞肺癌(NSCLC)中的表达及其与肺癌血管生成的关系。方法:应用免疫组织化学S-P法检测P-AKT、血管内皮细胞生长因子(VEGF)以及微血管密度(MVD)在46例NSCLC组织中的表达,并分析三者的表达与NSCLC临床病理特征的关系以及三者之间的相关性。结果:NSCLC中P-AKT、VEGF的阳性率分别为43.5%和67.4%,明显高于正常肺组织的0%和22.2%(P<0.05)。P-AKT的表达与肺癌的分化程度、分期、淋巴结转移密切相关(P<0.05)。VEGF的表达与肺癌的分期、淋巴结转移密切相关(P<0.05)。肺癌、正常肺组织中MVD值分别为24.62±6.21和13.26±5.96,两者相比,差异有统计学意义(P<0.05)。MVD值的高低与肺癌的分期、转移、分化程度密切相关(P<0.05)。P-AKT在肺癌中的表达与VEGF和MVD值密切相关(P<0.05)。结论:P-AKT在肺癌组织中的表达显著增高,并与肺癌的分期、转移和分化相关,P-AKT可以通过促进肺癌血管的生成导致肺癌的转移。 Objective: To investigate the levels of microvessel density(MVD), the expression of P-AKT and vascular endothelial growth factor(VEGF) in non-small cell lung cancer (NSCLC), and explore the correlation between them and the clinicopathological features of NSCLC. Methods: MVD and expressions of P-AKT and VEGF in 46 specimens of NSCLCS tissues and 18 specimens of normal lung tissues were detected by SP immunohistochemistry. Their interrelations and correlations were analyzed. Results: Positive rate of P-AKT and VEGF were significantly higher in NSCLC than in normal lung tissues (43.5% vs 0% and 67.4% vs 22.2%, P 〈 0.05) ; there were correlations between P-AKT expression and lymph node metastasis, between the TNM stage and differentiation of NSCLC ( P 〈 0.05) and between VEGF expression and lymph node metastasis and the TNM stage of NSCLC( P 〈 0.05). The MVD of lung cancer tissues was higher than that of normal lung tissues(24.62 ±6.21 vs13.26± 5.96, P 〈 0.05) ; there were correlations between the MVD and lymph node metastasis and between the TNM stage and differentiation of NSCLC ( P 〈 0.05). There were positive correlations between P-AKT expression and VEGF expression and MVD( P 〈0.05). Conclusion: P-AKT is over-expressed in NSCLC, which correlates with lymph node metastasis, the TNM stage and differentiation of NSCLC and takes part in the angiogenesis of NSCLC.
作者 高锡刚 王玲
出处 《山东大学学报(医学版)》 CAS 北大核心 2007年第2期184-187,191,共5页 Journal of Shandong University:Health Sciences
关键词 非小细胞肺 蛋白激酶类 血管内皮细胞生长因子 微血管密度 Carcinoma, non-small-cell lung Protein kinases Vascular endothelial growth factor Microvessel density
  • 相关文献

参考文献12

  • 1周晓东,于皆平,于红刚,罗和生,吕农华,朱萱.蛋白激酶B在胃癌中的表达及其生物学意义[J].中华消化杂志,2005,25(7):401-405. 被引量:21
  • 2Evaluation of two phosphorylation sites improve the prognostic significance of AKT activation in no-small-cell lung cancer tumors[J].Journal of Clinic Oncology,2006,24(2):306-314.
  • 3Vlom M,Koomagi R,Mattren J.Prognostic value of vascular endothelial growth factor and its receptor Flt-lin squamous cell lung cancer[J].Int J Cancer,1997,74(1):64-68.
  • 4Noel Weidner.Intra tumor microvessel density as a prognostis factor in cancer[J].Am J Pathol,1995,147(1):9-19.
  • 5Arboleda MJ,Lyons JF,Kabbinavar FF,et al.Overexpression of AKT2/protein kinase Bbeta leads to up-regulation of beta1 integrins,increased invasion,and metastasis of human breast and ovarian cancer cells[J].Cancer Res,2003,63(1):196-206.
  • 6Brognard J,Clark AS,Ni Y,et al.Akt/protein kinase B is constitutively active in non-small cell lung cancer cells and promotes cellular survival and resistance to chemotherapy and radiation[J].Cancer Res,2001,61(10):3 986-3 997.
  • 7Tang JM,He QY,Guo RX,et al.Phosphorylated Akt overexpression and loss of PTEN expression in non-small cell lung cancer confers poor prognosis[J].Lung Cancer,2006,51(2):181-191.
  • 8苗丽君,王静.Akt与肿瘤的研究进展[J].国外医学(生理病理科学与临床分册),2004,24(5):406-409. 被引量:38
  • 9Dimmeler S,Zeiher AM.Akt takes center stage in angiogenesis signaling[J].Circ Res,2000,86(1):4-5.
  • 10Zhong H,Chiles K,Feldser D,et al.Modulation of hypoxia inducible factor 1alpha expression by the epidermal growth factor/phosphatidylinositol 3-kinase/ PTEN/ AKT/FRAP pathway in human prostate cancer cells:implications for tumor angiogenesis and therapeutics[J].Cancer Res,2000,60(6):1 541-1 545.

二级参考文献36

  • 1Dudek H, Datta SR, Franke TF, et al. Regulation of neuronal survival by the serine-threonine protein kinase Akt. Science,1997,275:661-665.
  • 2Burgering BM, Coffer PJ. Protein kinase B(c-Akt) in phosphatidylinositol-3-OH kinase signal transduction. Nature,1995,376: 599-602.
  • 3Schlieman MG, Fahy BN, Ramsamooj R, et al. Incidence,mechanism and prognostic value of activated AKT in pancreas cancer. Br J Cancer, 2003,89:2110-2115.
  • 4Ringel MD, Hayre N, Saito J, et al. Overexpression and overactivation of Akt in thyroid carcinoma. Cancer Res, 2001, 61:6105-6111.
  • 5Itoh N, Semba S, Ito M, et al. Phosphorylation of Akt/PKB is required for suppression of cancer cell apoptosis and tumor progression in human colorectal carcinoma. Cancer, 2002,94:3127-3134.
  • 6Liu AX, Testa JR, Hamilton TC, et al. AKT2, a member of the protein kinase B family, is activated by growth factors,v-Ha-fas, and v-src through phosphatidylinositol 3-kinase in human ovarian epithelial cancer cells. Cancer Res, 1998, 58:2973-2977.
  • 7Sambrook J, Fritsch EF, Maniatis T, eds Molecular cloning: A laboratory manual, 2nd ed. New York: Cold Spring Harbor Laboratory Press, 1989.
  • 8Perez-Tenorio G, Stal O. Activation of AKT/PKB in breast cancer predicts a worse outcome among endocrine treated patients. Br J Cancer, 2002,86:540-545.
  • 9Terakawa N, Kanamori Y, Yoshida S. Loss of PTEN expression followed by Akt phosphorylation is a poor prognostic factor for patients with endometrial cancer. Endocr Relat Cancer,2003, 10:203-208.
  • 10Fresno Vara JA, Casado E, de Castro J, et al. PI3K/Akt signalling pathway and cancer. Cancer Treat Rev, 2004, 30: 193-204.

共引文献57

同被引文献57

引证文献6

二级引证文献38

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