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非小细胞肺癌组织中AKT2、CyclinD1、MMP-9表达及其与临床病理因素的关系 被引量:22

Expression of AKT2, Cyclin D1, and MMP-9 and Their Correlations to Clinicopathologic Features of Non-small Cell Lung Cancer
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摘要 背景与目的:AKT2是一种丝氨酸/苏氨酸激酶,已被确定为癌基因,在多种肿瘤组织中都存在AKT2的异常表达和活化,AKT2与肿瘤的增殖和侵袭转移密切相关。本研究旨在探讨AKT2、CyclinD1、MMP-9在非小细胞肺癌(non-smallcelllungcancer,NSCLC)中的表达及与临床病理因素的关系。方法:应用免疫组化的方法检测68例NSCLC组织、38例相应的癌旁组织和14例非肿瘤性肺组织标本中AKT2蛋白、CyclinD1、MMP-9的表达,采用!2检验分析临床病理因素与上述指标的相关性。结果:AKT2、CyclinD1、MMP-9在NSCLC组织中阳性率分别为91.2%、76.5%、72.1%,显著高于癌旁及非肿瘤性肺组织中阳性率(3.8%、0%、13.5%)(P<0.05)。AKT2的表达与患者年龄、性别、肿瘤类型及分化程度、TNM分期无关(P>0.05),与淋巴结转移有关(P<0.05)。CyclinD1、MMP-9表达与淋巴结转移、鳞癌的分化程度有关(P<0.05),MMP-9还与TNM分期有关(P<0.05)。AKT2的表达与CyclinD1、MMP-9呈正相关。结论:AKT2、CyclinD1、MMP-9均与肺癌的发展有关,CyclinD1、MMP-9的高表达可能与AKT2的调节有关。 BACKGROUND & OBJECTIVE: AKT2, a serine/threonine kinase, is confirmed to be an oncogene. Abnormal expression and activation of AKT2 is observed in many kinds of tumor tissues. AKT2 is associated with the proliferation and invasion of cancers. This study was designed to investigate the expression of AKT2, Cyclin D1, and matrix metalloproteinase- 9 (MMP-9) in human non-small cell lung cancer (NSCLC) tissue and their correlations to clinicopathologic features of NSCLC. METHODS. The expression of AKT2, Cyclin D1, and MMP-9 in 68 specimens of NSCLC, 38 specimens of corresponding adjacent tissues, and 14 specimens of nocancerous lung tissue were assessed by immunohistochemistry; their correlations to clinicopathologic factors were analyzed using Chi-square test. RESULTS. The positive rates of AKT2, Cyclin D1, and MMP-9 were significantly higher in NSCLC than in adjacent tissues and no-cancerous lung tissues (91.2% vs. 3.8%, 76.5% vs. 0%, 72.1% vs. 13.5%, P〈0.05). The expression of AKT2 wasn't correlated to age, sex, histologic subtype and differentiation, and TNM stage of NSCLC patients (P〉0.05), but was correlated to lymph node metastasis (P〈0.05). The expression of Cyclin D1 and MMP-9 was correlated to lymph node squamous cell carcinoma (P 〈0.05); correlated to TNM stage. The expression the expression of Cyclin D1 and MMP-9 metastasis and the expression differentiation of of MMP-9 was of AKT2 was positively correlated to (P〈0.05). CONCLUSIONS. AKT2, Cyclin D1, and MMP-9 is related to development of lung cancer. The overexpression of Cyclin D1 and MMP-9 may relate to AKT2 regulation.
出处 《癌症》 SCIE CAS CSCD 北大核心 2006年第1期69-72,共4页 Chinese Journal of Cancer
基金 教育部"211工程"重点学科建设项目~~
关键词 肺肿瘤 非小细胞性 AKT2 CYCLIN D1 MMP-9 Lung neoplasms Cancer, non-small cell AKT2 Cyclin D1 MMP-9
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参考文献8

  • 1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
  • 2YUAN Z Q, SUN M, FELDMAN R I, et al. Frequent activation of AKT2 and induction of apoptosis by inhibition of phosphoinositide-3-OH kinase/Akt pathway in hunmn ovarian cancer [J ]. Oncogene, 2000, 19(19) : 2324-2330.
  • 3VIVANCO I, SAWYERS C L. The phosphatidylinositol 3-kinase AKT pathway in human cancer [J]. Nat Rev Cancer,2002,2(7) :489-501.
  • 4ARBOLEDA M J, LYONS J F, KABBINAVAR F F, et al.Overexpression of AKT2/prntein kinase Bbeta leads to upregulation of betal integrins, increased invasion, and metastasis of human breast and ovarian caneer cells [J].Cancer Res, 2003,63 ( 1 ) : 196-206.
  • 5XU X, SAKON M, NAGANO H, et al. Akt2 expression correlates with prognosis of human hepatncellular carcinoma[J ]. Oneol Rep, 2004, 11 ( 1 ) : 25-32.
  • 6LIN X, BOHLE A S, DOHRMANN P, et al. Overexpression of phosphatidylinositol 3-kinase in human lung cancer [J].Langenbecks Arch Surg, 2001,386(4) : 293-301.
  • 7GAO N, FLYNN D C, ZHANG Z, et al. G1 cell cycle progression and the expression of G1 cyclins ate regulated by PI3K/AKT/mTOR/p70S6K1 signaling in human ovarian cancer cells [J]. Am J Physiol Cell Physiol, 2004,287(2):C281-291.
  • 8KIM D, KIM S, KOH H, et al. Akt/PKB promotes cancer cell invasion via increased motility and metalloproteinase production [J]. FASEB J, 2001,15( 11 ) : 1953-1962.

二级参考文献20

  • 1Potter C J, Pedraza LG, Xu T. Akt regulates growth by directly phosphorylating Tsc2 [ J ]. Nat Cell Biol, 2002,4 (9) :658-665.
  • 2Vander Heiden MG, Plas DR, Rathmell JC, et al . Growth factors can influence cell growth and survival through effects on glucose metabolism[J]. Mol Cell Biol, 2001 ,21 (17) :5899-5912.
  • 3Edinger AL, Thompson CB. Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake [ J ]. Mol Biol Cell,2002 , 13 (7) : 2276-2288.
  • 4West KA, Brognard J, Clark AS, et al. Rapid Akt activation by nicotine and a tobacco carcinogen modulates the phenotype of normal human airway epithelial cells [ J]. J Clin Invest, 2003,111(1) :81-90.
  • 5Nam SY, Jung GA, Hur GC, et al. Upregulation of FLIP(S) by Akt, a possible inhibition mechanism of TRAIL-induced apoptosis in human gastric cancers [ J ]. Cancer Sci, 2003,94 ( 12 ) : 1066-1073.
  • 6Gagnon V, St-Germain ME, Parent S, et al. Akt activity in endometrial cancer cells: regulation of cell survival through cIAP-1 [ J].Int J Oncol, 2003 ,23(3) :803-810.
  • 7Dan HC, Sun M, Kaneko S, et al. Akt Phosphorylation and Stabilization of X-linked Inhibitor of Apoptosis Protein (XIAP) [ J ]. J Biol Chem, 2004,279(7) :5405-5412.
  • 8Zhang D, Brodt P. Type 1 insulin-like growth factor regulates MT1-MMP synthesis and tumor invasion via PI3-kinase/Akt signaling[J]. Oncogene, 2003,22(7) :974-982.
  • 9Qian Y, Corum L, Meng Q, et al. PI3K induced actin filament remodeling through Akt and p70S6K1 : implication of essential role in cell migration [ J ]. Am J Physiol Cell Physiol, 2004,286 ( 1 ) :C153-C163.
  • 10Kim D, Kim S, Koh H, et al. Akt/PKB promotes cancer cell invasion via increased motility and metalloproteinase production [ J ].FASEB J, 2001,15 ( 11 ) : 1953-1962.

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