PTEN和MDM2在非小细胞肺癌中的表达及临床意义

目的：研究PTEN和MDM2在非小细胞肺癌（NSCLC）发生发展中的临床意义。方法：采用免疫组化SP法检测56例非小细胞肺癌组织及20例正常肺组织中PTEN和MDM2蛋白的表达。结果：56例肺癌组织中PTEN表达率为48.21%（27/56）,20例正常肺组织中PTEN表达率为95%（19/20）,二者有统计学意义（p〈0.05）。PTEN表达率与肿瘤的分化程度、临床分期、淋巴结转移有关（p〈0.05）。56例肺癌组织中MDM2表达率为53.57%（30/56）,20例正常肺组织MDM2表达率为10%（2/20）,二者有统计学意义（p〈0.05）,MDM2表达率与肿瘤的分化程度、临床分期、淋巴结转移有关（p〈0.05）。在NSCLC中,PTEN和MDM2的表达呈负相关（p〈0.05）。结论：PTEN和MDM2的异常表达在非小细胞肺癌的发生发展过程中起着重要的作用。     

PTEN 和MDM2 在非小细胞肺癌中的表达及临床意义

目的:研究PTEN和MDM2在非小细胞肺癌(NSCLC)发生发展中的临床意义。方法:采用免疫组化SP法检测56例非小细胞肺癌组织及20例正常肺组织中PTEN和MDM2蛋白的表达。结果:56例肺癌组织中PTEN表达率为48.21%(27/56),20例正常肺组织中PTEN表达率为95%(19/20),二者有统计学意义(p<0.05)。PTEN表达率与肿瘤的分化程度、临床分期、淋巴结转移有关(p<0.05)。56例肺癌组织中MDM2表达率为53.57%(30/56),20例正常肺组织MDM2表达率为10%(2/20),二者有统计学意义(p<0.05),MDM2表达率与肿瘤的分化程度、临床分期、淋巴结转移有关(p<0.05)。在NSCLC中,PTEN和MDM2的表达呈负相关(p<0.05)。结论:PTEN和MDM2的异常表达在非小细胞肺癌的发生发展过程中起着重要的作用。     

Searching cell-secreted proteomes for potential urinary bladder tumor markers

To search for biomarkers critical for bladder carcinoma diagnosis and prognosis, secreted proteomes of highly malignant U1 and pre-malignant U4 cell lines were initially analyzed. Proteins in the culture media of the U1 and U4 cell lines were systematically examined by SDS-PAGE combined with MALDI-TOF MS. Among them, expression of pro-u-plasminogen activator (pro-u-PA) was confirmed by Western blot analysis and further evaluated. In analyzing urine samples from bladder cancer patients and normal subjects, we established a statistically significant relationship between the low level and absence of pro-u-PA in urine with high stages and grades of the tumor samples. Constitutive expression of Ras dominant negative protein led to increased expression of pro-u-PA in culture media, indicating that the loss of pro-u-PA is associated with oncogenic transformation. Analysis of cancer-secreted proteomes can be a feasible, non-invasive and efficient strategy for searching potential bladder tumor biomarkers. Our work also has identified the loss of pro-u-PA in urine as potential marker of more advanced bladder carcinoma.     

DDX5、E-cadherin在非小细胞肺癌中的表达及其临床意义

目的:探讨DEAD-box家族的DDX5(RNA解旋酶)和E-钙黏蛋白(E-cadherin)在非小细胞肺癌(NSCLC)组织中表达,并分析其临床病理意义。方法:采用免疫组织化学方法(SP法)和Western blot法检测手术切除的NSCLC组织74例及癌旁组织(距肿瘤5 cm)36例中DDX5和E-cadherin的表达情况,并对其与NSCLC患者的临床病理特征的相关性进行统计学分析。结果:NSCLC组织中DDX5的阳性表达率显著高于癌旁组织(63.5%vs 30.6%),E-cadherin的阳性表达率显著低于癌旁组织(60.8%vs 100%),差异均具有统计学意义(P0.05);DDX5和E-cadherin蛋白的表达水平与NSCLC的TNM分期以及淋巴结是否转移具有显著相关性(P0.05),但二者与NSCLC患者的年龄、性别和肿瘤组织类型均无显著相关性(P0.05)。DDX5和E-cadherin蛋白的表达呈显著负相关(r=-0.327,P0.05)。结论:DDX5的过度表达及E-cadherin的表达下调可能参与了NSCLC的发生发展,且二者在其中可能也具有相互作用的关系。     

SKIL facilitates tumorigenesis and immune escape of NSCLC via upregulating TAZ/autophagy axis

Immune escape is an important mechanism in tumorigenesis. The aim of this study was to investigate roles of SKIL in tumorigenesis and immune escape of non-small-cell lung cancer (NSCLC). SKIL expression levels in NSCLC cell line, clinical sample, and adjacent normal tissue were measured by quantitative PCR, western blot, or immunohistochemistry. Lentivirus was used to overexpress/silence SKIL or TAZ expression. Malignant phenotypes of NSCLC cells were evaluated by colony formation, transwell, and MTT assays, and in xenograft mice model. Syngeneic mice model and flow cytometry were used to evaluate T cell infiltration. Quantitative PCR and western blot were applied to evaluate relevant mRNA and protein levels, respectively. Co-immunoprecipitation was applied to unveil the interaction between SKIL and TAZ. SKIL expression was higher in NSCLC tissue compared to adjacent normal tissue. Silencing of SKIL inhibited malignant phenotypes of NSCLC cells and promoted T cell infiltration. SKIL-knockdown inhibited autophagy and activated the STING pathway in NSCLC cells through down-regulation of TAZ. Silencing of TAZ cancelled the effects of SKIL overexpression on malignant phenotypes and autophagy of NSCLC cells. Inhibition of autophagy reversed the effects of SKIL/TAZ overexpression on the STING pathway. In conclusion, SKIL promoted tumorigenesis and immune escape of NSCLC cells through upregulation of TAZ/autophagy axis and inhibition on downstream STING pathway.Subject terms: Immunology, Cancer     

Livin 蛋白在非小细胞肺癌中的表达及其临床意义

目的：研究livin 蛋白在非小细胞肺癌中的表达及其与非小细胞肺癌的生物学特性及临床预后的关系。方法：通过免疫组化 的方法检测和比较88 例非小细胞肺癌组织和20例癌旁正常肺组织中livin 蛋白的表达,并分析其与非小细胞肺癌的临床病理特 征和预后的相关性。结果：非小细胞肺癌组织及癌旁正常肺组织中livin 蛋白的阳性表达率分别为54.55%和5%,差异有显著统计 学差异(P<0.05)。非小细胞肺癌组织中livin 蛋白的表达水平与淋巴结转移、TNM分期显著相关(P<0.05),但与患者的性别、年龄、 分化程度及病理学类型无关(P>0.05)。Livin 高表达的非小细胞肺癌患者生存时间显著短于livin 低表达的患者(P<0.05)。结论： Livin 蛋白在非小细胞肺癌的发生及发展中起重要作用并与患者的预后相关,可能作为非小细胞肺癌新的防治靶点。     

ILK在肺鳞状细胞癌和肺腺癌的表达及其与临床病理特征和预后的关系

目的 探讨ILK在肺鳞状细胞癌和肺腺癌组织中的表达情况,及其与病理分型、肿瘤分化、分期、淋巴结转移及预后的关系。方法采用S-P免疫组织化学方法和Western Blot法,检测肺鳞状细胞癌和肺腺癌组织及相应癌旁肺组织中整合连接激酶（integrin-linkedkinase,ILK）的表达情况,并结合临床和病理资料进行分析。结果免疫组化结果显示：ILK在53／76（70％）的肺癌组织中阳性表达。其中鳞状细胞癌阳性率75％（33／44）,腺癌阳性率62．5％（20／32）,其表达与肺鳞状细胞癌的分化呈负相关（P〈0．01）,与临床分期（P〈0．01）、淋巴结转移（P〈0．01）呈正相关;与肺腺癌的临床分期（P〈0．01）和淋巴结转移（P〈0．01）正相关,与分化程度无相关性（P〉0．05）。同时,其表达与患者的生存时间呈负相关（P〈0．01）,与年龄、性别、肿瘤大小和组织类型等因素无关。Western Blot法进一步证实ILK在肺癌组织中的表达显著高于癌旁正常肺组织（P〈0．01）,其表达与肺癌的分化（P〈0．01）显著负相关。结论肺鳞状细胞癌和肺腺癌中,ILK与肺癌的侵袭和转移有关。ILK可作为判断肺鳞状细胞癌和肺腺癌预后的参考指标。     

Differentially expressed and activated proteins associated with non small cell lung cancer tissues

Background

Lung cancer is a leading cause of mortality. The most common cancer subtype, non small cell lung cancer (NSCLC), accounts for 85-90 % all cases and is mainly caused by environmental and genetic factors. Mechanisms involved in lung carcinogenesis include deregulation of several kinases and molecular pathways affecting cell proliferation, apoptosis and differentiation. Despite advances in lung cancer detection, diagnosis and staging, survival rate still remains poor and novel biomarkers for both diagnosis and therapy need to be identified. In the present study, we have explored the potential of novel specific biomarkers in the diagnosis of NSCLC, and the over-expression/activation of several kinases involved in disease development and progression.

Method

Lung tumor tissue specimens and adjacent cancer-free tissues from 8 NSCLC patients undergoing surgery were collected. The differential activation status of ERK1/2, AKT and IKBα/NF-κβ was analyzed. Subsequently, protein expression profile of NSCLC vs normal surrounding tissue was compared by a proteomic approach using LC-MS MS. Subsequently, MS/MS outputs were analyzed by the Protein Discoverer platform for label-free quantitation analysis. Finally, results were confirmed by western blotting analysis.

Results

This study confirms the involvement of ERK1/2, AKT, IKBα and NF-κβ proteins in NSCLC demonstrating a significant over-activation of all tested proteins. Furthermore, we found significant differential expression of 20 proteins (R_sc ≥ 1.50 or ≤ −1.50) of which 7 are under-expressed and 13 over-expressed in NSCLC lung tissues. Finally, we validated, by western blotting, the two most under-expressed NSCLC tissue proteins, carbonic anhydrase I and II isoforms.

Conclusion

Our data further support the possibility of developing both diagnostic tests and innovative targeted therapy in NSCLC. In addition to selective inhibitors of ERK1/2, AKT, IKBα and NF-κβ, as therapeutic options, our data, for the first time, indicates carbonic anhydrase I and II as attractive targets for development of diagnostic tools enabling selection of patients for a more specific therapy in NSCLC.     

Identification of isocitrate dehydrogenase 1 as a potential diagnostic and prognostic biomarker for non-small cell lung cancer by proteomic analysis

Lung cancer is the leading cause of cancer-related death in the world. To explore tumor biomarkers for clinical application, two-dimensional fluorescence difference gel electrophoresis and subsequent MALDI-TOF/TOF mass spectrometry were performed to identify proteins differentially expressed in 12 pairs of lung squamous cell tumors and their corresponding normal tissues. A total of 28 nonredundant proteins were identified with significant alteration in lung tumors. The up-regulation of isocitrate dehydrogenase 1 (IDH1), superoxide dismutase 2, 14-3-3ε, and receptor of activated protein kinase C1 and the down-regulation of peroxiredoxin 2 in tumors were validated by RT-PCR and Western blot analysis in independent 15 pairs of samples. Increased IDH1 expression was further verified by the immunohistochemical study in extended 73 squamous cell carcinoma and 64 adenocarcinoma clinical samples. A correlation between IDH1 expression and poor overall survival of non-small cell lung cancer (NSCLC) patients was observed. Furthermore, ELISA analysis showed that the plasma level of IDH1 was significantly elevated in NSCLC patients compared with benign lung disease patients and healthy individuals. In addition, knockdown of IDH1 by RNA interference suppressed the proliferation of NSCLC cell line and decreased the growth of xenograft tumors in vivo. These observations suggested that IDH1, as a protein promoting tumor growth, could be used as a plasma biomarker for diagnosis and a histochemical biomarker for prognosis prediction of NSCLC.     

UNC5A,an epigenetically silenced gene,functions as a tumor suppressor in non-small cell lung cancer

UNC5A has been reported to be related with human cancers. However, the function and mechanism in non-small cell lung carcinoma (NSCLC) remains unknown. We analyzed two NSCLC cell lines (A549 and H157), one normal human bronchial epithelial cell line (BEAS-2B) and the tissues of NSCLC. We used quantitative real-time PCR (qRT-PCR), western blot and immunohistochemical (IHC) staining to examine the expression of UNC5A. Methylation status of the UNC5A promoter was analyzed using methylation-specific PCR (MSP) and bisulfite sequencing PCR (BSP). We used western blot to analyzed protein levels of PI3K/Akt pathway. We found that the mRNA expression of UNCA5 was significantly downregulated in NSCLC cells and tissues. The promoter of UNC5A was hypermethylated in NSCLC cells compared to normal control cells. The expression of UNC5A could be reversed by demethylation agent in NSCLC cells. The expression of UNC5A was decreased in NSCLC samples and significantly associated with the advanced types of NSCLC. Functionally, knockdown of UNC5A promoted cell proliferation, migration, invasion and induced apoptosis in NSCLC, overexpression of UNC5A yielded the opposite result. Moreover, we found that UNC5A negatively regulated PI3K/Akt signaling pathway in NSCLC. UNC5A is a novel epigenetically silenced gene in NSCLC and consequent under-expression of UNC5A may contribute to NSCLC tumorigenesis through regulating PI3K/Akt pathway.     

Proteomic profiling of endothelial cells in human lung cancer

Genomic and proteomic analysis of normal and diseased tissues have yielded an abundance of molecular information for diagnostic and potential therapeutic targets. Changing the target of analysis from poorly accessible cells within tissues to easily accessible vascular endothelium has theoretical advantages in tissue-specific targeting. In this study, we sought to map a large-scale proteome of microvascular endothelium in human non-small cell lung cancer (NSCLC) and normal lung tissues, and identify lung cancer-related endothelial cell (EC)-selective proteins. Endothelial cells were isolated within NSCLC tissues and adjacent-normal lung tissue of lung cancer patients by using CD31-immunomagnetic beads. The complex proteins from the ECs were separated by one-dimensional gel electrophoresis, and the proteins in each gel band were digested by trypsin. Peptides were separated by online reverse-phase liquid-chromatography and analyzed by electrospray ionization (ESI) ion trap tandem mass spectrometry. Approximately 600-1000 proteins were identified in each individual sample. Five patient cases of paired individual data, extracted from the protein identification data sets of both normal- and cancer-derived ECs, were analyzed by subtractive proteomics. An average of 300 proteins was specifically identified from each lung cancer-derived EC isolate, compared to normal lung-derived ECs. With the use of several comparative analyses, we identified among those 300 proteins, 16 common candidate proteins that were detected in at least 3 of 5 cases specific to lung cancer-derived ECs. Proteins selectively identified in cancer-derived ECs, including coatomer protein complex, subunit gamma (COPG), and peroxiredoxin 4 (PRDX4), were validated by Western blot analysis. In an additional experiment in which 16 cancer samples were analyzed by immunohistochemistry, PRDX4, thymopoietin (TMPO), and COPG were confirmed to be abundantly expressed in lung cancer-derived ECs and in cancerous lung cells. Further ongoing analysis of these 16 candidate proteins will determine their potential applicability to NSCLC-specific diagnosis and therapeutics.     

METTL3通过上调ING5抑制非小细胞肺癌细胞增殖

目的:探讨METTL3在非小细胞肺癌中的表达及作用,并探讨其可能的机制。方法:通过慢病毒转染,在HCC827细胞中过表达和敲除METTL3,并通过免疫印迹验证METTL3蛋白表达。免疫印迹检测HCC827细胞中生长抑制物家族成5(Methyltransferase Like 3,甲基转移酶3)调控ING5(Inhibitor Of Growth Family Member 5,METTL3)。使用基因表达交互分析(Gene Expression Profiling Interactive Analysis,GEPIA)探究了METTL3和ING5在非小细胞肺癌组织和正常组织中的表达相关性。用CCK-8法检测METTL3和ING5表达对非小细胞肺癌细胞增殖的影响。使用KM-plotter验证METTL3、ING5的表达与非小细胞肺癌的总生存期(OS)、进展后生存期(PPS)和无进展生存期(PFS)之间的相关性。结果:免疫印迹结果显示,在HCC827细胞中METTL3过表达上调了ING5蛋白的表达,而METTL3表达下调了ING5蛋白的表达。GEPIA数据库分析显示METTL3在非小细胞肺癌中的表达明显低于正常组织(P<0.05)。CCK-8检测结果显示,与对照组相比METTL3缺失促进了HCC827细胞的增殖能力,而METTL3过表达显著抑制了HCC827细胞的增殖能力。此外,METTL3通过ING5调控非小细胞肺癌细胞的增殖能力。KM-plotter分析显示METTL3、ING5 m RNA的表达与非小细胞肺癌患者的生存有较好的预后关系。结论:METTL3在非小细胞肺癌低表达,并通过调控ING5的表达在非小细胞肺癌的发生进展中发挥重要地抑癌基因作用。     

p16和Ki67在非小细胞肺癌组织中的表达及其与预后的关系

目的探讨p16和Ki67在非小细胞肺癌（non-small cell lung cancer,NSCLC）中的表达,研究它们对NSCLC患者预后的影响及其与临床及病理因素之间的关系。方法收集NSCLC术后标本160例及正常肺组织20例（对照组）,应用免疫组化法检测NSCLC组织和正常肺组织中p16和Ki67的表达。结果在NSCLC组织和正常肺组织中,p16和Ki67的阳性表达率分别为23.8%、82.5%和90%、5%,差异有统计学意义（P〈0.05）。多因素分析：PTNM分期、淋巴结转移、p16及Ki67的表达是影响NSCLC根治术后患者预后的独立因素（P〈0.05）;p16阳性组与阴性组5年生存率分别为55.3%和18.0%,差异有统计学意义（P〈0.05）;Ki67阳性组与阴性组5年生存率分别为23.5%和42.9%,差异有统计学意义（P〈0.05）,p16和Ki67表达呈负相关（P〈0.05）。结论 p16和Ki67参与了NSCLC的发生发展,p16和Ki67的表达水平与NSCLC的发展及预后有一定的关系。     

CREB和CXCR2在非小细胞肺癌组织中的表达及意义

目的：探讨c AMP反应原件结合蛋白（cyclic AMP response element-binding protein,CREB）和CXC趋化因子受体2（CXC chemokine receptor 2,CXCR2）在非小细胞肺癌（non-small cell lung cancer,NSCLC）组织中的表达及与肺癌发生、发展的关系。方法：采用免疫组化Elivision法检测CREB和CXCR2在49例NSCLC组织中的表达,同时随机选取20例癌旁正常肺组织作为对照。结果：NSCLC中CREB和CXCR2的表达阳性率分别为57.1%和69.4%,均显著高于癌旁正常组织中的10.0%和15.0%（P〈0.05）;同时,CREB和CXCR2在NSCLC组织中的表达不仅与肿瘤的TNM分期有关（P〈0.05）,而且还与肿瘤的分化程度有关（P〈0.05）;另外,CREB在吸烟患者中的表达明显高于非吸烟患者（P〈0.05）,在鳞癌组织中的表达明显高于腺癌（P〈0.05）;CREB和CXCR2的表达呈正相关。结论：CREB和CXCR2可能参与了NSCLC的发生和发展,为NSCLC的靶向治疗提供了新的依据。     

Livin蛋白在非小细胞肺癌中的表达及其临床意义

目的：研究livin蛋白在非小细胞肺癌中的表达及其与非小细胞肺癌的生物学特性及临床预后的关系。方法：通过免疫组化的方法检测和比较88例非小细胞肺癌组织和20例癌旁正常肺组织中livin蛋白的表达,并分析其与非小细胞肺癌的临床病理特征和预后的相关性。结果：非小细胞肺癌组织及癌旁正常肺组织中livin蛋白的阳性表达率分别为54．55％和5％,差异有显著统计学差异（P〈0．05）。非小细胞肺癌组织中livin蛋白的表达水平与淋巴结转移、TNM分期显著相关（P〈O．05）,但与患者的性别、年龄、分化程度及病理学类型无关（P〉0．05）。Livin高表达的非小细胞肺癌患者生存时间显著短于livin低表达的患者（P〈0．05）。结论：Livin蛋白在非小细胞肺癌的发生及发展中起重要作用并与患者的预后相关,可能作为非小细胞肺癌新的防治靶点。     

AIMP3 inhibits cell growth and metastasis of lung adenocarcinoma through activating a miR-96-5p-AIMP3-p53 axis

Aminoacyl-tRNA synthetase-interacting multifunctional protein-3 (AIMP3) is a tumour suppressor, however, the roles of AIMP3 in non-small cell lung cancer (NSCLC) are not explored yet. Here, we reported that AIMP3 significantly inhibited the cell growth and metastasis of NSCLC (lung adenocarcinoma) in vitro and in vivo. We have firstly identified that AIMP3 was down-regulated in human NSCLC tissues compared with adjacent normal lung tissues using immunohistochemistry and western blot assays. Overexpression of AIMP3 markedly suppressed the proliferation and migration of cancer cells in a p53-dependent manner. Furthermore, we observed that AIMP3 significantly suppressed tumour growth and metastasis of A549 cells in xenograft nude mice. Mechanically, we identified that AIMP3 was a direct target of miR-96-5p, and we also observed that there was a negative correlation between AIMP3 and miR-96-5p expression in paired NSCLC clinic samples. Ectopic miR-96-5p expression promoted the proliferation and migration of cancer cells in vitro and tumour growth and metastasis in vivo which partially depended on AIMP3. Taken together, our results demonstrated that the axis of miR-96-5p-AIMP3-p53 played an important role in lung adenocarcinoma, which may provide a new strategy for the diagnosis and treatment of NSCLC.     

波形蛋白在非小细胞肺癌组织中的表达及其临床意义

目的:探究波形蛋白在非小细胞肺癌(NSCLC)组织中的表达及其与肺癌浸润转移的相关性。方法:收集2012年6月-2014年6月我院手术切除的NSCLC癌组织标本150例及癌旁正常组织(距肿瘤5 cm)79例,提取两组的RNA,采用实时荧光定量聚合酶链反应(RT-PCR)检测波形蛋白m RNA表达水平,免疫组化法检测波形蛋白的蛋白表达,分析波形蛋白表达水平与淋巴结转移、TNM分期的相关性。结果:波形蛋白m RNA在NSCLC癌组织中的表达明显高于癌旁正常组织(P0.05)。NSCLC癌组织中波形蛋白m RNA表达水平的上调与淋巴结转移及TNM分期(P0.05)相关。结论:波形蛋白在NSCLC患者中表达异常升高,与NSCLC的发生和浸润转移密切相关。     

Proteomics Approaches for Identification of Tumor Relevant Protein Targets in Pulmonary Squamous Cell Carcinoma by 2D-DIGE-MS

Potential markers for progression of pulmonary squamous cell carcinoma (SCC) were identified by examining samples of lung SCC and adjacent normal tissues using a combination of fluorescence two-dimensional difference gel electrophoresis (2D-DIGE), matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS), and electrospray ionization quadrupole-time of flight mass spectrometry (ESI-Q-TOF). The PANTHER System was used for gel image based quantification and statistical analysis. An analysis of proteomic data revealed that 323 protein spots showed significantly different levels of expression (P≤0.05) in lung SCC tissue compared to expression in normal lung tissue. A further analysis of these protein spots by MALDI-TOF-MS identified 81 different proteins. A systems biology approach was used to map these proteins to major pathways involved in numerous cellular processes, including localization, transport, cellular component organization, apoptosis, and reproduction. Additionally, the expression of several proteins in lung SCC and normal tissues was examined using immunohistochemistry and western blot. The functions of individual proteins are being further investigated and validated, and the results might provide new insights into the mechanism of lung SCC progression, potentially leading to the design of novel diagnostic and therapeutic strategies.     

非小细胞肺癌中血管生成拟态和VEGF的表达及意义

目的探讨血管生成拟态(vasculogenic mimicry,VM)与血管内皮生长因子(vascular epithelial growth factor,VEGF)在非小细胞肺癌(non-small cell lung cancer,NSCLC)中的表达及意义。方法收集NSCLC术后标本160例和20例正常肺组织,应用免疫组化法和组织化学法检测NSCLC和正常肺组织中VM和VEGF的表达情况。结果在NSCLC组织和正常肺组织中,VM和VEGF的阳性率分别为36.9%、51.3%和0%、0%,差异有统计学意义;含有VM的NSCLC的VEGF表达高于无VM者(P<0.05),且VM与NSCLC的组织学分级、淋巴结转移及临床分期等有关(P<0.05);多因素分析:PTNM分期、VM、VEGF的表达是影响NSCLC根治术后患者预后的独立因素(P<0.05);VM阳性组与阴性组的5年生存率分别为1.7%和41.6%,差异有统计学意义;VEGF阳性组与阴性组的5年生存率分别为2.4%和52.6%,差异有统计学意义。结论具有VM的NSCLC组织分化低,患者临床预后差;VEGF的表达水平和VM与NSCLC的发展及预后有一定的关系。