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食管鳞癌组织中磷酸化表皮生长因子受体和Akt蛋白的表达 被引量:10

Expressions of p-EGFR and p-Akt proteins in esophageal squamous cell carcinoma tissue
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摘要 目的:探讨磷酸化表皮生长因子受体(p-EGFR)及其下游信号磷酸化蛋白激酶Akt(p-Akt)在食管鳞癌组织中的表达及其相关性。方法:采用免疫组化法检测50例食管鳞癌组织和50例相应癌旁正常食管黏膜组织中p-EGFR和p-Akt蛋白的表达,并分析二者与食管鳞癌患者临床病理特征的关系以及二者在食管鳞癌组织中表达的相关性。结果:食管癌组织中p-EGFR和p-Akt蛋白表达水平均高于癌旁正常食管黏膜组织(χ2配对=9.818和33.390,P<0.05)。p-EGFR和p-Akt蛋白的表达与食管鳞癌的分化程度(χ2=18.083和11.049,P<0.05)、淋巴结转移(χ2=7.284和5.817,P<0.05)有关,与患者的性别、肿瘤直径及TNM分期无关(P>0.05)。此外,p-EGFR和p-Akt蛋白在食管鳞癌中的表达呈正关联(rP=0.501,P<0.001)。结论:p-EGFR和p-Akt蛋白的高表达可能与食管鳞癌的恶性程度密切相关。 Aim: To investigate the expressions of phosphorylated epidermal growth factor receptor( p-EGFR) and its downstream signaling phosphorylated Akt( p-Akt) in esophageal squamous cell carcinoma( ESCC) tissue and their correlation.Methods: Immunohistochemistry was utilized to detect the expressions of p-EGFR and p-Akt proteins in 50 cases of ESCC tissue and matched normal esophageal epithelial tissue,and their correlation in ESCC tissue was investigated.Results: The expressions of p-EGFR and p-Akt proteins in ESCC tissue were significantly higher than those in normal esophageal epithelial tissue( χ^2paired= 9.818 and 33.390,P〈 0.05).Additionally,the expressions of p-EGFR and p-Akt proteins in ESCC tissue with poor differentiation and lymph node metastasis were markedly higher than those in ESCC tissue with high differentiation( χ^2= 18.083 and 11.049,P〈 0.05) and without lymph node metastasis( χ^2= 7.284 and 5.817,P〈 0.05),however,the ex-pressions of p-EGFR and p-Akt proteins were not related to the patients' gender,tumor size or TNM staging( P〈 0.05).Moreover,the expressions of p-EGFR and p-Akt proteins in ESCC tissue displayed positive correlation( r P= 0.501,P〈 0.001).Conclusion: p-EGFR and p-Akt proteins at high level may be closely associated with the malignant degree of ESCC.
出处 《郑州大学学报(医学版)》 CAS 北大核心 2015年第1期5-8,共4页 Journal of Zhengzhou University(Medical Sciences)
基金 河南省科技攻关基金资助项目112102310090
关键词 食管鳞癌 表皮生长因子受体 AKT 磷酸化 esophageal squamous cell carcinoma epidermal growth factor receptor Akt phosphorylation
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  • 1Lurje G,Lenz HJ. EGFR signaling and drug discovery[ J]. Oncology, 2009,77 (6) :400.
  • 2Hammarsten P, Rudolfsson SH, Henriksson R, et al. Inhibi- tion of the epidermal growth factor receptor enhances cas- tration-induced prostate involution and reduces testoster- one-stimulated prostate growth in adult rats [ J ]. Prostate, 2007,67 (6) :573.
  • 3Mimeauh M,Batra SK. Frequent gene products and molec- ular pathways altered in prostate cancer-and metastasis-ini- tiating cells and their progenies and novel promising multi- targeted therapies [ J ]. Mol Med, 2011, ! 7 ( 9/10 ) :949.
  • 4Del Peso L, Gonzalez-Garcia M, Page C, et al. Interleukin- 3-induced phosphorylation of BAD through the protein ki- nase Akt[ J]. Science, 1997,278 (5338) :687.
  • 5Lin HK ,Yeh SY, Kang HY, et al. Akt suppresses androgen- induced apoptosis by phosphorylating and inhibiting andro- gen receptor[ J]. Proc Natl Acad Sci USA ,2001,98 ( 13 ) : 7200.
  • 6An SJ,Lin QX, Chen ZH, et al. Combinations of laminin 5 with PTEN,p-EGFR and p-Akt define a group of distinct molecular subsets indicative of poor prognosis in patients with non-small cell lung cancer[ J]. Exp Ther Med,2012,4 (2) :226.
  • 7Wallerand H, Cai Y, Wainberg ZA, et al. Phospho-Akt pathway activation and inhibition depends on N-cadherin or phospho-EGFR expression in invasive human bladder canc- er cell lines [ J ]. Urol Onco1,2010,28 ( 2 ) : 180.
  • 8Tateishi K ,Ichiyama T, Hirai K ,et al. ClinieM outcomes in elderly patients administered gefitinib as first-line treatment in epidermal growth factor receptor-mutated non-small-celllung cancer:retrospective analysis in a Nagano Lung Canc- er Research Group Study [ J ]. Med Oncol, 2013,30 ( 1 ) : 450.
  • 9Crvenkova S, lvkovski L, Dimovski A, et al. Effectiveness of erlotinib as a second line therapy for patients with epider- mal growth factor receptor (EGFR) mutation in non-small cell lung cancer ( NSCLC ) : our clinical experience [ J ]. Prilozi, 2012,33 ( 1 ) : 303.
  • 10] Licitra L, Stfirkel S, Kerr KM, et al. Predictive value of epidermal growth factor receptor expression for first-line chemotherapy plus cetuximab in patients with head and neck and colorectal cancer:analysis of data from the EX- TREME and CRYSTAL studies [ J ]. Eur J Cancer,2013, 49(6) :1161.

同被引文献98

  • 1李月白,胡新永,王义生.地塞米松和辛伐他汀对成骨细胞增殖分化的影响[J].郑州大学学报(医学版),2006,41(6):1072-1075. 被引量:4
  • 2郑学芝,刘桂莲,李丽,孙卫,念红,胡静,蔡子微.RNA干扰Nucleostemin基因对人食管癌Eca-109细胞株增殖影响的实验研究[J].肿瘤防治研究,2007,34(2):103-105. 被引量:5
  • 3金春亭,鲁蓓,李海军,李玉珍,武欣,范婕,张林西.环氧化酶-2选择性抑制剂抑制人食管癌细胞的生长及其诱导凋亡[J].世界华人消化杂志,2007,15(5):440-446. 被引量:7
  • 4Pass DP,Carbone DH,Johnson,et al.Principles and practice of lung cancer:the offical reference text of the LASLC[M].4th ed.Philadelphia:Lippincott Williams&Wilkins,2010:287-324.
  • 5Yang H,Bi Y,Xue L.Multifaceted modulation of SIRT1in cancer and inflammation[J].Crit Rev Oncog,2015,20(1/2):49-64.
  • 6Debelec-Butuner B,Ertunc N,Korkmaz KS.Inflammation contributes to NKX3.1loss and augments DNA damage but does not alter the DNA damage response via increased SIRT1expression[J].J Inflamm(Lond),2015,12:12.
  • 7Gao R,Chen J,Hu Y,et al.Sirt1 deletion leads to enhanced inflammation and aggravates endotoxin-induced acute kidney injury[J].PLoS One,2014,9(6):e98909.
  • 8Gao R,Ma Z,Hu Y,et al.Sirt1 restrains lung inflammasome activation in a murine model of sepsis[J].Am J Physiol Lung Cell Mol Physiol,2015,308(8):L847-853.
  • 9Ge L,Shi R.Progress of EGFR-TKI and ALK/ROS1inhibitors in advanced non-small cell lung cancer[J].Int J Clin Exp Med,2015,8(7):10330-10339.
  • 10Tan CS,Gilligan D,Pacey S.Treatment approaches for EGFR-inhibitor-resistant patients with non-small-cell lung cancer[J].Lancet Oncol,2015,16(9):e447-459.

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