子宫颈鳞状细胞癌中GDF-15与EMT相关蛋白的表达及相关性

目的检测子宫颈鳞状细胞癌组织中GDF-15及上皮-间质转化(epithelial-mesenchymal transition, EMT)相关蛋白E-cadherin、N-cadherin、vimentin的表达,探讨GDF-15在子宫颈鳞状细胞癌发生、侵袭中的生物学作用。方法采用免疫组化EliVision两步法检测85例子宫颈鳞状细胞癌组织及其配对癌旁子宫颈组织中GDF-15、E-cadherin、N-cadherin、vimentin的表达,分析GDF-15表达与子宫颈鳞状细胞癌临床病理特征的关系及GDF-15与EMT相关蛋白表达的相关性。结果与癌旁子宫颈组织相比,子宫颈鳞状细胞癌组织中GDF-15、N-cadherin和vimentin表达上调,E-cadherin表达下调,差异有统计学意义(P均0.05)。子宫颈鳞状细胞癌组织中GDF-15表达与N-cadherin和vimentin表达呈正相关(r_s=0.422,r_s=0.374),与E-cadherin表达呈负相关(r_s=-0.305)。结论 GDF-15与EMT相关蛋白在子宫颈鳞状细胞癌组织中异常表达,过表达GDF-15在子宫颈癌的发生、侵袭中发挥重要作用,可能与诱导子宫颈癌EMT有关。     

Livin表达与胃癌上皮-间质转化的关系及临床意义

目的探讨Livin表达与胃癌上皮-间质转化(epithelial-mesenchymal transition,EMT)的关系及临床意义。方法采用免疫组化法检测110例胃癌及相应癌旁正常胃组织中Livin和EMT标志蛋白的表达,分析Livin表达与胃癌临床病理特征的关系及Livin表达与EMT标志蛋白表达的相关性。应用Western blot法检测8例新鲜胃癌组织中Livin和EMT标志蛋白的表达。结果胃癌组织中Livin阳性率(59. 1%)明显高于相应癌旁组织(8. 2%)(P 0. 05)。Livin表达与胃癌淋巴结转移相关(P 0. 001)。Western blot检测结果显示Livin在有淋巴结转移的胃癌组中表达高于无淋巴结转移组。胃癌组织中E-cadherin、vimentin和N-cadherin的阳性率分别为29. 1%、30. 9%和57. 3%。胃癌组织中Livin与E-cadherin的表达呈负相关(r=-0. 322,P=0. 001),与vimentin和N-cadherin的表达呈正相关(r=0. 276,P=0. 004; r=0. 216,P=0. 024)。Livin高表达的胃癌组织中,vimentin和N-cadherin亦高表达,而E-cadherin表达降低,反之亦然。结论 Livin表达与胃癌组织的EMT表型有关,并促进胃癌的转移。     

舌鳞状细胞癌中Survivin的表达及与上皮细胞-间质转化的关系

目的探讨Survivin在舌鳞状细胞癌(tongue squamous cell carcinoma,TSCC)中的表达及其与上皮细胞-间质转化(epithelial-mesenchymal transition,EMT)的关系。方法采用免疫组化EnVision法检测63例TSCC及相应癌旁正常组织中Survivin和EMT标志物的表达,分析Survivin表达与TSCC临床病理特征的关系及其与EMT标志物的相关性。应用Western blot法检测8例TSCC新鲜组织中Survivin、E-cadherin和N-cadherin的表达。结果TSCC组织中Survivin阳性率为81.0%,明显高于相应癌旁正常组织中(15.9%);Survivin表达与TSCC临床分期、病理分级及淋巴结转移有明显相关性。E-cadherin和N-cadherin在TSCC组织中阳性率分别为42.9%和69.8%;Survivin与E-cadherin的表达呈负相关,与N-cadherin表达呈正相关。Western blot实验结果也证实,Survivin和N-cadherin在TSCC组织中呈高表达,而E-cadherin呈低表达。结论Survivin表达与TSCC组织EMT标志物有关,Survivin可能通过诱导TSCC细胞发生EMT,从而促进TSCC的侵袭和转移。     

PDCD5通过Wnt/β-catenin通路抑制肾细胞癌侵袭转移及其机制研究

目的探讨肾细胞癌(RCC)患者PDCD5的表达水平及其参与调控RCC侵袭与转移的可能机制。方法利用免疫组化检测RCC标本与癌旁组织中PDCD5的蛋白表达水平,同时分析PDCD5与疾病分期、预后的相关性;利用transwell及划痕实验检测PDCD5对肾癌细胞系A498侵袭与转移的影响;利用Western blot检测A498细胞转染PDCD5后MMP2、MMP9、E-cadherin、N-cadherin及Wnt/β-catenin通路的变化。结果 (1)与癌旁组织相比,RCC标本中PDCD5明显下调(P0.001),且与疾病分期及预后正相关;(2)PDCD5明显抑制了肾癌细胞系A498的转移与侵袭能力(P0.01);(3)PDCD5通过抑制A498细胞系中MMP2、MMP9及N-cadherin的表达水平,增强E-cadherin的表达水平调控EMT转化,同时Wnt/β-catenin通路关键蛋白下调。结论 PDCD5通过调控Wnt/β-catenin通路影响肾细胞癌EMT转化,负性调控了RCC病人的侵袭与转移进程。     

透明细胞肾细胞癌中FOXD1的表达及其对786-O细胞增殖侵袭、上皮-间质转化的影响

目的 探讨转录因子FOXD1在透明细胞肾细胞癌(clear cell renal cell carcinoma, CCRCC)组织和细胞系中的表达及其对786-O细胞增殖侵袭、上皮-间质转化(epithelial-mesenchymal transition, EMT)的影响。方法 采用qRT-PCR技术检测CCRCC组织和细胞系中FOXD1基因表达，并分析FOXD1表达与CCRCC临床病理特征及预后的关系；检测敲低FOXD1表达对786-O细胞生物学行为和EMT相关标志物表达的影响。结果 CCRCC组织中FOXD1的表达量(0.917 2±0.096 58)高于对照组(0.556 9±0.074 82),差异有统计学意义(P<0.05)。肿瘤TNM分期、淋巴结转移及FOXD1高表达均为CCRCC患者预后相关的独立危险因子(P<0.05)。下调FOXD1基因发现，CCRCC细胞系786-O的体外侵袭与增殖活性明显减弱(P<0.05)。与对照组相比，敲低FOXD1表达后N-cadherin、Ki-67和vimentin表达下调(P<0.05),E-cadherin...     

三阴型乳腺癌中PD-L1的表达与上皮-间质转化的关系及意义

目的探讨三阴型乳腺癌(triple-negative breast cancer, TNBC)中PD-L1表达与上皮-间质转化(epithelial-mesenchymal transition, EMT)的关系及临床意义。方法采用免疫组化EnVision两步法检测PD-L1在125例TNBC肿瘤浸润性免疫细胞中的表达,EMT标志蛋白(E-cadherin、vimentin)在125例TNBC组织及50例癌旁组织中的表达,分析三种蛋白与TNBC临床病理学特征的关系及PD-L1表达与EMT标志蛋白的相关性。结果 TNBC组织中E-cadherin的阳性率(52.80%)低于癌旁组织(90.00%)(P0.05),vimentin阳性率(41.60%)高于癌旁组织(16.00%)(P0.05);TNBC中PD-L1与E-cadherin蛋白表达呈负相关(χ~2=17.440,P0.05);PD-L1与vimentin蛋白表达呈正相关(χ~2=6.253,P=0.012);PD-L1、E-cadherin和vimentin的表达均与淋巴结转移、Ki-67增殖指数、组织学分级有关(P0.05)。结论 TNBC中PD-L1表达异常增高,且与癌细胞中EMT表型相关,两者可能在肿瘤发生、发展中具有协同作用。     

结肠癌组织中LKB1的表达及其与上皮-间质转化的关系

目的探讨LKB1在结肠癌组织中的表达及其与肿瘤上皮-间质转化的关系。方法采用免疫组化法检测75例结肠癌组织及对应癌旁正常结肠组织中LKB1、上皮-间质转化(epithelial mesenchymal transformation,EMT)相关标志物E-cadherin、N-cadherin、vimentin的表达,分析LKB1表达与结肠癌临床病理特征及EMT的关系。结果 49例结肠癌组织中LKB1低表达,55例正常结肠组织中LKB1高表达;LKB1表达降低与淋巴结转移、TNM肿瘤分期相关(P0.05);E-cadherin、N-cadherin、vimentin分别在25例、48例、26例结肠癌组织中高表达,LKB1表达与E-cadherin表达呈正相关(r=0.648,P0.05),与Ncadherin(r=-0.891,P0.05)和vimentin(r=-0.660,P0.05)表达呈负相关。结论 LKB1在结肠癌组织中表达下调,与EMT的发生呈正相关,可作为结肠癌转移发生的预测指标。     

转移相关基因FMNL2参与胃癌侵袭转移的相关性分析

目的探讨转移相关基因FMNL2与胃腺癌上皮-间质转化(epithelial-mesenchymal transitions,EMT)的关系,为胃癌转移机制提供新线索。方法收集20例正常胃黏膜、92例胃腺癌、43例淋巴结转移癌组织进行免疫组化分析,比较3种组织标本中FMNL2和E-cadherin、CK、vimentin的阳性率,分析FMNL2表达与胃癌EMT的关系。结果FMNL2、vimentin在胃腺癌中的表达明显高于正常胃黏膜组织;在淋巴结转移癌中的表达高于胃腺癌组织(P0.05)。上皮标志物E-cadherin、CK在正常黏膜中的表达显著高于胃腺癌及淋巴结组织(P0.05)。相关性分析发现FMNL2与E-cadherin、CK呈负相关(r=-0.466,P=0.000,r=-0.327、P=0.000);与vimentin表达呈正相关(r=0.553,P=0.000)。结论 FMNL2与胃腺癌EMT相关,并可能通过EMT促进胃腺癌侵袭转移。     

体外肺癌上皮-间充质转化三维模型的建立及其对顺铂抵抗的机制研究

目的:探索转化生长因子β1(transforming growth factor-β1,TGF-β1)诱导三维培养肺癌细胞发生上皮-间充质转化(epithelial-mesenchymal transition,EMT)及对顺铂抵抗的相关机制。方法:用荧光倒置显微镜、扫描电镜及激光共聚焦观察人非小细胞肺癌细胞系95D在TGF-β1刺激前后的形态及蛋白表达变化,Western blot检测三维培养95D细胞在TGF-β1刺激前后相关蛋白表达变化,MTT法检测95D细胞发生EMT前后对顺铂的敏感性变化。结果:在三维培养条件下,95D细胞在TGF-β1刺激后,细胞球出现塌陷、细胞离散、迁移等现象,细胞球之间互相融合。激光共聚焦结果显示95D细胞在TGF-β1刺激后,E-cadherin蛋白表达无变化,N-cadherin和vimentin蛋白表达显著上调。Western blot结果显示,在TGF-β1刺激后,95D细胞的E-cadherin蛋白表达下调(P<0.05),N-cadherin和vimentin蛋白表达上调(P<0.05),p-AKT和p-mTOR蛋白水平升高(P<0.05)。而LY294002和rapamycin可逆转TGF-β1诱导的上述蛋白表达(P<0.05)。MTT结果显示,TGF-β1刺激组对顺铂的敏感性显著低于普通三维培养组(P<0.01),而LY294002和rapamycin增强TGF-β1刺激后95D细胞对顺铂的敏感性(P<0.01)。结论:TGF-β1诱导三维培养肺癌细胞发生EMT及对顺铂抵抗,可能是通过激活PI3K/AKT/mTOR信号通路实现的。     

上皮-间质转化在蒿甲醚逆转结直肠癌细胞放化疗抵抗中的作用

目的:探讨上皮-间质转化(epithelial-mesenchymal transition,EMT)在蒿甲醚(artemether,ARE)对同期放化疗抵抗人结直肠癌细胞HCT116(HCT1 16CRR)的逆转作用中的作用.方法:实验分为四组:1)对照组;2)单纯放化疗组;3)ARE联合放化疗组;4)ARE组.采用Real-time PCR和Westernblot,检测各组EMT相关指标E-cadherin,N-cadherin,vimentin,snail mRNA及其蛋白的表达情况.结果:Real-time PCR和Western blot结果显示E-cadherin mRNA及其蛋白的表达情况,单纯放化疗组＜ARE联合放化疗组＜对照组＜ARE组;N-cadherin,vimentin,snail mRNA及其蛋白的表达情况,单纯放化疗组＞ARE联合放化疗组＞对照组＞ARE组.结论:EMT在ARE逆转同期放化疗抵抗人结直肠癌细胞HCT116CRR细胞系的放化疗抵抗作用中有重要的作用,即上调E-cadherin mRNA及其蛋白的表达,下调N-cadherin,vimentin,snail mRNA及其蛋白的表达.     

High expression of E-cadherin in pleural effusion cells predicts better prognosis in lung adenocarcinoma patients

Background: Epithelial-mesenchymal transition (EMT) is of great importance in tumor metastasis. Our previous study demonstrates that epithelial phenotype is related to epidermal growth factor receptor (EGFR) mutation and the sensitivity of EGFR tyrosine kinase inhibitors (TKIs) in advanced non-small cell lung cancer (NSCLC) patients. However, the role of EMT phenotype in malignant pleural effusions in predicting prognosis is unknown in lung adenocarcinoma patients. Method: Pleural effusions of lung adenocarcinoma patients were collected and made into cell block (CB). EGFR mutation was detected using amplification refractory mutation system (ARMS) PCR method and H-score system was applied to evaluate the staining intensity of EMT marker and tumor cell ratio. Results: Forty-three CB samples, including 22 samples before any treatment (baseline, group 1) and 21 with disease progression (group 2) after first-line chemotherapy, were enrolled in this study. The expression of N-cadherin and vimentin were low in the CB tumor cells. There was no significant difference in the tumor cell radio and E-cadherin expression in the two groups. E-cadherin expression had no association with sex, age and smoking status and also patient response in both the two groups. However, high E-cadherin expression was related to EGFR mutation (P = 0.032) and long progression-free survival (PFS) (P = 0.015) in group 1 but not group 2 samples. Conclusion: E-cadherin expression in CB samples was associated with EGFR mutation status and patient prognosis in lung adenocarcinoma patients in first-line chemotherapy.     

含微乳头结构肺腺癌CT重建征象特征及上皮间质转化相关基因表达

目的 探讨含微乳头结构（MPP）肺腺癌具有的CT重建征象特征,上皮间质转化（EMT）相关分子表达情况以及它们之间的关系。 方法 选取含MPP侵袭性肺腺癌（IAC）37例、不含MPP 80例及其对应的癌旁组织,比较临床病理特征、CT重建征象;应用Real-time PCR及Western blotting检测EMT有关标识分子表达变化情况。 结果 含MPP组淋巴结转移比例较高、毛刺、胸膜凹陷征、实性及分叶比例较高（均P<0.001）。 含MPP组E-钙黏蛋白（cadherin）及β-连环蛋白（β-catenin）表达均下调（P<0.05）,N-cadherins、波形蛋白（vimentin）、Snail及转化生长因子（TGF）-β表达均上调（P<0.05）。有毛刺组E cadherin及β-catenin表达下调者所占比例较高,而vimentin表达上调者所占比例较高（均P<0.05）;实性结节组E-cadherin表达下调者所占比例较高,而N-cadherin及vimentin表达上调者所占比例较高（均P<0.05）。 结论 含MPP浸润性肺腺癌具有特征性CT重建征象,发生了EMT改变。其CT重建征象与EMT相关分子表达存在联系。     

TGF-β1诱导大鼠肝星状细胞系HSC-T6活化及上皮间质转换

目的探讨转化生长因子-β1(TGF-β1)在大鼠肝星状细胞系(HSC-T6)活化及上皮间质转换(EMT)中的作用。方法体外培养HSC-T6,用MTT法筛选TGF-β1对HSC-T6作用的最佳浓度;用10μg/L TGF-β1处理HSC-T6 24 h,相差倒置显微镜下观察细胞形态改变,免疫荧光染色法检测细胞骨架结构F-actin蛋白的表达,RT-q PCR法检测肌动蛋白α-SMA及代表上皮间质转换的神经黏附素(N-cadherin)、波形蛋白(vimentin)和上皮黏附素(E-cadherin)基因表达;用不同浓度(0、5和10μg/L)的TGF-β1处理HSC-T6 24 h,Western blot检测α-SMA、N-cadherin、vimentin和E-cadherin蛋白表达。结果 10μg/L TGF-β1干预HSC-T6 24 h有最好的细胞存活率;TGF-β1刺激HSC-T6后,细胞拉伸,伪足增多呈星形,细胞间连接疏松,呈显著活化状态;F-actin聚集形成应力纤维丝,沿细胞长轴分布;实验组α-SMA mRNA及vimentin mRNA的表达量明显高于对照组(P0.05),而E-cadherin mRNA的表达量明显降低(P0.05);在不同浓度的TGF-β1呈剂量依赖性致α-SMA及N-cadherin和vimentin的蛋白表达量增多,而E-cadherin的蛋白表达量减少。结论 TGF-β1可诱导HSC-T6活化及上皮间质转换。     

SphK1和FAK对人结肠癌HCT116细胞上皮间质转化的影响

 目的: 研究鞘氨醇激酶1(sphingosine kinase l,SphK1)和黏着斑激酶(focal adhesion kinase,FAK)对人结肠癌HCT116细胞上皮间质转化(epithelial-mesenchymal transition,EMT)的影响。方法: 将人结肠癌HCT116细胞分成3组:采用SphK1抑制剂N,N-二甲基鞘胺醇(N,N-dimethylsphingosine,DMS)、FAK抑制剂PF573228和相同体积的培养基分别处理细胞。MTT法检测细胞活力,Western blot方法检测SphK1、FAK、E-cadherin、N-cadherin、vimentin和基质金属蛋白酶2(MMP2)蛋白的表达,real-time PCR检测SphK1、鞘氨醇1-磷酸(S1P)、FAK、E-cadherin和vimentin mRNA的表达,并应用细胞划痕实验检测肿瘤细胞的迁移能力。结果: PF573228和DMS均明显抑制人结肠癌HCT116细胞的活力,并呈时间剂量依赖性。DMS抑制SphK1的表达,同时下调FAK、N-cadherin、vimentin和MMP2蛋白的表达,而上调E-cadherin蛋白表达上调。PF573228明显抑制FAK的表达,同时抑制SphK1、N-cadherin、vimentin和MMP2的表达,上调E-cadherin蛋白的表达(P<0.01)。划痕实验显示PF573228和DMS显著抑制HCT116细胞的迁移能力(P<0.01)。与对照组比较,PF573228组和DMS组FAK、SphK1、S1P以及vimentin mRNA的表达明显下调,而E-cadherin mRNA的表达则明显上调(P<0.05)。结论: SphK1和FAK信号通路可能在结肠癌HTC116细胞上皮间质转化过程中发挥重要作用。     

川楝素对人卵巢癌细胞侵袭和迁移的影响

目的:探讨川楝素(toosendanin,TSN)对人卵巢癌细胞迁移和侵袭能力的影响及相关机制。方法:用不同浓度川楝素处理人卵巢癌CAVO-3和SKVO-3细胞,采用CCK-8法检测TSN处理12、24、48、72和96 h后的细胞存活率;通过细胞划痕实验和Transwell小室侵袭实验检测TSN对人卵巢癌细胞的迁移和侵袭能力的影响;采用Western blot法检测核因子κB(NF-κB)p65、上皮型钙黏蛋白(E-cadherin)、神经型钙黏蛋白(N-cadherin)、波形蛋白(vimentin)和Snail蛋白的表达情况。结果:TSN抑制CAVO-3和SKVO-3细胞活力(P0.05)。与对照组相比,TSN组CAVO-3细胞的迁移和侵袭能力明显降低,且NF-κB p65和E-cadherin表达升高,N-cadherin、vimentin和Snail表达下降(P0.05);而加入NF-κB抑制剂BAY11-7082至TSN处理的细胞后明显逆转了以上效应,与TSN组相比,TSN+BAY11-7082组CAVO-3细胞的迁移和侵袭能力显著升高,且E-cadherin表达下降,N-cadherin、vimentin和Snail表达升高(P0.05)。结论:川楝素能抑制人卵巢癌细胞的迁移和侵袭能力,其机制可能与抑制由NF-κB/Snail信号通路所介导的上皮-间充质转化过程有关。     

二苯乙烯苷通过PI3K/AKT通路抑制TGFβ诱导的结直肠癌上皮间质转换

目的:探讨二苯乙烯苷(2,3,5,4'-tetrahydroxy stilbene-2-Ο-β-D-glucoside,THSG)对TGFβ诱导的结直肠癌细胞上皮间质转换(epithelial-mesenchymal transition,EMT)的影响及可能的分子机制.方法:通过转化生长因子(transforming growth factorβ,TGFβ)诱导HCT116细胞发生EMT,倒置显微镜观察细胞形态变化,Western印迹检测EMT相关分子标志物的表达;划痕实验、细胞迁移实验、倒置显微镜观察不同浓度THSG干预TGFβ刺激对HCT116细胞运动、迁移能力以及形态学的影响,Western印迹检测EMT相关标志物及PI3K/AKT通路的改变.结果:TGFβ刺激HCT116细胞后,细胞由圆形变为长梭形,E-cadherin表达降低,vimentin和N-cadherin表达增加;与对照组相比,THSG可增加E-cadherin和PTEN的表达,降低vimentin和N-cadherin和p-AKT表达,同时抑制细胞的迁移及运动(F=454.723,P<0.001;F=412.161,P<0.001).结论:THSG可通过PI3K/AKT通路抑制TGFβ诱导的HCT116细胞EMT,并降低其运动迁移能力.     

紫草素对HGF诱导的人肺癌细胞上皮-间充质转化的逆转作用

目的:探讨紫草素(shikonin)对肝细胞生长因子(HGF)诱导的人非小细胞肺癌PC9细胞迁移、侵袭及上皮-间充质转化(EMT)的影响。方法:用HGF诱导PC9细胞建立EMT模型,采用不同剂量的shikonin干预24 h后,MTT法检测细胞活力;划痕愈合实验检测细胞的迁移能力;Transwell小室实验检测细胞的侵袭能力;Western blot法检测细胞中上皮型钙黏蛋白(E-cadherin)、神经型钙黏蛋白(N-cadherin)和波形蛋白(vimentin)的蛋白表达水平。结果:Shikonin可显著抑制PC9细胞的活力(P0.01),随着给药剂量的增加,shikonin对细胞的生长抑制率显著上升,并呈一定的剂量依赖关系,IC_(50)为9.364μmol/L。HGF可诱导PC9细胞发生迁移和侵袭;划痕愈合实验和Transwell小室实验显示,shikonin能明显抑制由HGF诱导的肺癌PC9细胞迁移和侵袭(P0.01)。Western blot检测结果显示HGF可诱导PC9细胞的EMT标志物E-cadherin蛋白表达下调,N-cadherin和vimentin蛋白表达上调,使其发生EMT;shikonin则可逆转由HGF诱导的PC9细胞E-cadherin蛋白表达下调及N-cadherin和vimentin蛋白表达上调(P0.01)。结论:Shikonin能逆转由HGF诱导的肺癌PC9细胞EMT,同时抑制其迁移和侵袭。     

Expression of E-cadherin and vimentin in oral squamous cell carcinoma

The aim of the study is to determine the levels of E-cadherin, vimentin expression in tumor tissues from patients with oral squamous cell carcinoma (OSCC), and the relationship between the expression of E-cadherin, vimentin and epithelial-mesenchymal transition, in order to explore its values for predicting the invasion and metastasis of oral squamous cell carcinoma, short survival of patients in many types of cancer. E-cadherin and vimentin expression of 10 benign and 42 OSCC tumor tissues was examined by immunohistochemical staining. E-cadherin is positively expressed in normal oral mucosa epithelium, but vimentin expression is not found in normal oral mucosa epithelia; the E-cadherin and vimentin were expressed in 26 of 42 (61.9%) and 16 of 42 (38.1%), respectively. No statistically difference was found for E-cadherin and vimentin expression in patients with different age, gender and tumor location, E-cadherin and vimentin expression was significantly associated with lymph node metastasis and tissue location (P < 0.05); E-cadherin expression was also significantly associated with tumor stage (P < 0.05); there are significantly difference between infiltrative margin and central area in patients with oral squamous cell carcinoma for E-cadherin and vimentin positive expression (P < 0.05). E-cadherin and vimentin positive expression was associated with tumor metastasis of oral squamous cell carcinoma. Our study preliminarily confirmed that EMT phenomenon is existed during the development of oral squamous cell carcinoma. Co-evaluation of E-cadherin and vimentin might be a valuable tool for predicting OSCC patient outcome.     

Expression of poly(C)-binding protein 1 (PCBP1) in NSCLC as a negative regulator of EMT and its clinical value

Poly (C)-binding Protein 1 (PCBP1) is a 35 kDa protein involved in a number of biological processes. Recently, the research found that PCBP1 might be involved in epithelial-mesenchymal transition (EMT). However, the role of PCBP1 in non-small-cell lung cancer (NSCLC) metastasis needs further elucidation. The purpose of this study was to determine whether PCBP1 could serve as a biomarker for stratification and prediction of prognosis in NSCLC as a regulator of EMT formation. In this study, PCBP1 expression was evaluated by Western blot in 8 fresh lung cancer tissues and immunohistochemistry (IHC) on 145 paraffin-embedded slices. PCBP1 was highly expressed in non-metastatic NSCLC specimens and significantly correlated with lymph node status (P < 0.001), clinical stage (P = 0.001), vimentin expression (P = 0.033) and E-cadherin expression (P = 0.042). Our study showed that the low expression of PCBP1 was correlated with decreased expression of E-cadherin and elevated expression of vimentin, which were the markers of EMT. Besides, high expression of PCBP1 was correlated with better prognosis. These findings suggested that PCBP1 might play an important role in preventing the process of EMT in NSCLC, thus be a promising therapeutic target to inhibit NSCLC metastasis.