MT1-MMP反义核酸抑制高转移人卵巢癌SW626细胞的侵袭效应

背景与目的:MT1-MMP(MMP-14)是新发现的一种膜型基质金属蛋白酶,研究表明MT1-MMP在肿瘤转移中发挥关键性作用。本研究应用反义核酸技术,观察了MT1-MMP反义核酸对高转移人卵巢癌SW626细胞体外生长和侵袭的抑制效应。方法:应用自行设计的引物,借助RT-PCR技术获得两端含不同限制酶位点的MT1-MMPcDNA片段,反向插入pcDNA3.1中,并应用脂质体介导的基因转染技术,将重组质粒导入SW626细胞中,应用MTT、Westernblot、明胶酶谱和体外侵袭实验等方法观察了SW626细胞转染前后,细胞生长、MT1-MMP蛋白表达、MMP-2和MMP-9酶活性及细胞体外侵袭能力等指标的变化。结果:成功构建了反义MT1-MMP真核表达载体(pMMP14as),将其转染入SW626细胞后,与空质粒转染组相比,MT1-MMP反义核酸转染组细胞MT1-MMP表达显著降低,抑制率为65.8%;MMP-2酶原的活化受到明显抑制;pMMP14as转染组的穿膜细胞百分数为(63.3±5.8)%,明显低于空质粒转染组(97.6±7.5)(P<0.05)%。结论:MT1-MMP反义核酸可明显抑制高转移SW626细胞体外生长和侵袭效应,提示MT1-MMP可作为人卵巢癌抗侵袭治疗的分子靶点。     

卵巢癌细胞PCDGF的表达与意义

目的研究人卵巢癌细胞PCDGF的表达,探讨其与卵巢癌恶性表型的关系.方法应用半定量RT-PCR和Western blot分别检测3株卵巢癌细胞中PCDGF mRNA和蛋白表达水平.单层细胞增殖实验测定3株卵巢癌细胞的增殖能力;Boyden小室体外侵袭实验测定不同细胞株的侵袭能力.结果 3株卵巢癌细胞PCDGF转录和翻译水平呈同步变化(P<0.05),均为SW626最高,A2780稍低,Skov-3最低.而其增殖、侵袭能力亦为SW626最强, A2780次之, Skov-3最弱.结论 3株卵巢癌细胞PCDGF mRNA和蛋白表达水平与其增殖、侵袭能力呈正相关(前者r1=0.97, r2=0.89,后者r1=0.85,r2=0.84),提示PCDGF在卵巢癌发生演进中可能作为独立因素起多种作用,有望成为治疗的新靶点.     

反义端粒酶RNA对肝癌细胞黏附和侵袭的影响

目的:探讨人反义端粒酶RNA(human telomerase RNA,hTR)对肝癌细胞系BEL-7402黏附和侵袭的影响及其机制。方法:利用前期实验成功转染端粒酶正、反义RNA基因的肝癌细胞,分为正义转染组(BEL-7402-hTR-EcoRⅠ细胞)、反义转染组(BEL-7402-hTR-BamHⅠ细胞),空白对照组(BEL-7402细胞)。黏附实验和侵袭实验检测反义hTR转染后BEL-7402细胞的黏附和侵袭能力,免疫细胞化学检测整合素β1(integrinβ1,INTβ1)、上皮钙黏蛋白(epithelial cadherin,E-cad)的表达水平,明胶酶谱法检测基质金属蛋白酶(matrix metalloproteinase,MMP)-2、-9的活性变化。结果:与空白对照组和正义hTR转染组相比,反义hTR转染组BEL-7402-hTR-BamHⅠ细胞的黏附、侵袭能力明显减低(0.204±0.029vs0.505±0.037、0.465±0.029,34.80±3.19vs71.47±5.15、69.87±3.11,均P<0.05),INTβ1表达降低(0.153±0.016vs0.385±0.008、0.375±0.014,P<0.05),E-cad表达增强(0.209±0.020vs0.124±0.018、0.134±0.016,P<0.05),MMP-2和MMP-9的活性受到明显抑制(2 054.22±138.52vs3 105.56±329.60、2 923.22±269.08,846.33±104.66vs1 538.89±122.85、1 453.33±126.35,均P<0.05)。结论:人反义端粒酶RNA能明显减低肝癌BEL-7402细胞的黏附、侵袭能力,其机制可能与上调E-cad的表达、下调INTβ1的表达,并抑制MMP-2和MMP-9的活性有关。     

视黄酸依赖反义cyclin D1对HL-60细胞细胞周期素依赖性激酶的影响

目的探讨视黄酸(retinoic acid,RA)及其诱导的反义(anti-sense,AS)cyclin D1对HL-60细胞的细胞周期素激酶CDK4的影响.方法通过构建含有视黄酸反应元件(retinoic acid response element, RARE)的反义cyclin D1 RNA表达载体pCI-neo/RARE3-TK/Ascyclin D1,使反义cyclin D1的表达可受视黄酸诱导调控.以脂质体转染HL-60白血病细胞后,运用MTT比色法检测细胞增殖功能、NBT还原实验观测细胞分化状况,RT-PCR以及western-blot等方法观测视黄酸处理后CDK4的mRNA和蛋白表达水平的改变.结果 RA处理后,细胞生长显著减慢,分化能力明显增强,CDK4 mRNA和蛋白表达水平均有所降低,其中,以反义cyclin D1转染细胞经RA处理后变化更为显著.结论 RA及其诱导的反义cyclin D1对HL-60细胞的抑制增殖与诱导分化效应可能与CDK4表达下调有关.     

RNA干扰CTSL表达抑制卵巢癌细胞的侵袭和转移

目的：构建组织蛋白酶L基因(cathepsin L, CTSL)RNAi的真核表达载体,探讨干扰CTSL基因表达对卵巢癌细胞侵袭和转移的影响。方法：设计并合成4对CTSL小干扰RNA(small interfering RNA,siRNA),转染卵巢癌A2780细胞,RT-PCR检测各转染细胞CTSL的表达,筛选沉默效果最好的siRNA序列。设计并合成CTSL-shRNA序列,与psilence4.1-CMV-neo载体连接,构建psilence4.1-CTSL表达载体。psilence4.1-CTSL转染A2780细胞,获得稳定转染克隆A2780-CTSL。RT-PCR和Western blotting验证CTSL基因干扰效果,MTT法和集落形成实验检测A2780细胞的增殖,流式细胞术检测A2780细胞周期,Transwell侵袭小室实验检测A2780细胞体外侵袭和迁移能力。结果：筛选出干扰效果最好的siRNA-CTSL-1202序列,并成功构建相应的CTSL-shRNA表达载体psilence4.1-CTSL。稳定转染psilence4.1-CTSL能沉默A2780细胞中CTSL的表达。沉默CTSL基因后可抑制A2780细胞的侵袭和转移,但不影响A2780细胞的增殖、细胞周期和黏附活性。结论：成功构建CTSL基因siRNA的真核表达载体,RNA干扰CTSL基因表达可抑制卵巢癌细胞的侵袭和转移。     

RNAi抑制Akt2基因表达对卵巢癌细胞系A2780放射敏感性的影响

背景与目的:许多研究已经表明蛋白激酶B(P13K/Akt)在肿瘤细胞恶性增殖及肿瘤对放化疗的拮抗中起着重要作用,Akt2是Akt家族成员之一.本研究应用RNAi(RNA interference,RNAi)技术抑制Akt2基因的表达,观察其对肿瘤细胞生长和放射敏感性的影响.方法:构建Akt2基因的短发卡状RNA质粒转染人卵巢癌细胞A2780,同时以转染空载体和未转染组作为对照,3组细胞命名为pAkt2-shRNA/A2780,pEGFP/A2780和A2780)运用RT-PCR、蛋白质免疫印迹方法比较转染前后Akt2表达的差异;四甲基偶氮唑蓝实验绘制细胞生长曲线;克隆形成实验观察细胞的放射敏感性变化,以克隆形成率表示;6 MV X线10 Gy照射后48 h收集细胞,流式细胞仪(FACS)分析细胞凋亡情况.结果:与对照相比,shRNA可抑制Akt2 mRNA转录和蛋白的表达,差异显著(P＜0.05);pAkt2-shRNA/A2780细胞生长明显慢于pEGFP/A2780和A2780细胞;pAkt2-shRNA/A2780细胞克隆形成率明显低于pEGFP/A2780细胞和A2780细胞(P＜0.05);pAkt2-shRNA/A2780,pEGFP/A2780和A2780细胞凋亡率分别为(78.3±2.2)%、(41.2±1.8)%和(40.4±2.0)%,差异有显著性(P＜0.05).结论:转染针对Akt2基因shRNA真核表达载体,抑制卵巢癌细胞中Akt2基因表达,能抑制细胞增殖,促进细胞凋亡,增强其对放射治疗的敏感性.     

婆罗双树样基因2对A2780细胞生长及转移影响

目的 婆罗双树样基因2(sal-like gene 2,SALL2)作为肿瘤抑制基因,在多种肿瘤细胞的生长过程中发挥调控作用.本研究旨在探讨SALL2基因对卵巢癌(ovarian cancer,OC) A2780细胞生长和转移的影响.方法 采用小干扰RNA(small-interfering ribonucleic acid,siRNA)转染OC A2780细胞以沉默SALL2,设载体组及空白对照组.采用RT-PCR和蛋白质印迹法检测SALL2的表达.采用CCK-8和流式细胞术(flow cytometry,FCM)检测细胞增殖,采用FCM检测细胞凋亡.应用划痕实验检测细胞迁移,采用侵袭实验检测细胞侵袭.结果 A2780细胞高表达SALL2的mRNA及蛋白.RT-PCR结果显示,转染siRNA2和siRNA3 48 h后,空白对照组、载体组、siRNA2和siRNA3组平均2-△△Ct值分别为1.000±0.030、0.942±0.053、0.207±0.041和0.465±0.007,差异有统计学意义,F=8.213,P=0.024.转染siRNA2和siRNA3 48 h后,空白对照组、载体组及siRNA2和siRNA3组蛋白表达相对灰度比值分别为0.629±0.035、0.603±0.072、0.225±0.004和0.453±0.061,差异有统计学意义,F=11.629,P=0.018.siRNA2组转染72 h后的细胞增殖力(4.285±0.026)显著高于载体组(3.622±0.029)和空白对照组(3.614±0.016),差异有统计学意义,F=34.023,P=0.012.siRNA2组转染48 h后的细胞凋亡率为(49.17±2.03)％,显著低于载体组的(56.82±2.74)％和空白对照组的(58.39±2.45)％,差异有统计学意义,F=5.781,P=0.037.siRNA2组转染48 h后处于G0/G1期的细胞比例为(47.87±1.28)％,均显著低于载体组的(55.27±1.46)％与空白对照组的(56.60±1.57)％,差异有统计学意义,F=4.213,P=0.032.siRNA2组转染48 h后划痕愈合率为(78.925±6.133)％,明显高于载体组的(38.504±3.772)％和空白对照组的(42.169±4.103)％,差异有统计学意义,F=17.184,P=0.006.siRNA2组转染48 h后穿过基质胶的细胞数(147.169±7.208)显著高于载体组(92.169±11.052)和空白对照组(95.169±9.830),差异有统计学意义,F=12.698,P=0.014.结论 SALL2沉默促进A2780细胞增殖、迁移和侵袭,抑制细胞凋亡.     

反义c-met基因对人卵巢癌SKOV3细胞增殖侵袭的影响

目的:用构建的c-met反义质粒阻断肝细胞生长因子(hepatocytegrowthfactor,HGF)/c-met信号传导,探讨c-met信号传导阻滞对卵巢癌细胞增殖和侵袭的影响及其机制。方法:将c-met基因反向克隆入真核表达载体pcDNA3·1中,酶切鉴定结果。用脂质体法将c-met反义基因转染人卵巢癌SKOV3细胞,G418筛选获得阳性克隆,RT-PCR检测转染前后SKOV3细胞中c-met、基质金属蛋白酶-9(matrixmetalloproteinase-9,MMP-9)mRNA的表达,流式细胞仪检测转染前后SKOV3细胞中c-met和MMP-9蛋白阳性细胞数,应用细胞生长曲线和Boyden小室观察转染前后细胞的增殖和侵袭作用。结果:获得反向构建的c-met真核表达载体,c-met反义RNA转染卵巢癌细胞后,c-met和MMP-9mRNA分别减少0·24±0·03倍(P=0·001)和0·70±0·03倍(P=0·002);c-met和MMP-9蛋白阳性细胞率分别为(27·17±1·23)%和(17·32±0·46)%,较对照组(98·92±0·62)%和(36·47±2·94)%显著降低(P=0·000、0·007);卵巢癌细胞侵入基底膜的细胞数为4·5±1·5,较对照组(17±2·0)明显减少(P=0·000),细胞的增殖明显减慢。结论:c-met受体基因表达在卵巢癌生长和转移中起重要作用,阻断c-met的信号传导可以明显抑制卵巢癌细胞的增殖,降低肿瘤生长转移的能力,为卵巢癌的基因治疗提供了一定的实验依据。     

RhoC/ROCK-Ⅰ信号通路封闭对卵巢癌细胞生物学行为影响的研究

目的:探讨 RhoC/ROCK-Ⅰ信号转导通路的封闭对卵巢癌细胞体外生物学行为的影响.方法:RT-PCR及蛋白质印迹法检测RhoC及ROCK-Ⅰ在不同卵巢癌细胞系中mRNA及蛋白的表达水平;将ROCK-Ⅰ反义寡核苷酸(ASODN)转染人卵巢癌细胞系SW626与Caov-3细胞后,检测转染前后ROCK-Ⅰ蛋白的表达,Boyden小室观察各株细胞转染前后侵袭及运动能力的变化,MTT比色法测定转染前后黏附能力的变化.结果:RhoC和ROCK-Ⅰ在4种卵巢癌细胞中呈不同程度表达,其中RhoC的表达水平与癌细胞侵袭力和迁移能力呈正相关,r=0.95,P<0.01,转染ROCK-Ⅰ ASODN后,细胞内ROCK-Ⅰ的表达明显减少;细胞的侵袭能力受到明显的抑制,10 μmol/L组和20 μmol/L组SW626细胞的侵袭能力分别为对照组的(75.6±3.8)%和(54.7±2.9)%,Caov-3为(68.8±4.7)%和(50.0±4.5)%;转染两种浓度ASODN的SW626与Caov-3细胞的随机运动能力分别为对照组的(80.0±1.3)%、(63.7±1.9)%、(72.0±1.3)%和(55.9±2.5)%;定向运动能力分别为对照组的(83.9±1.4)%、(64.1±1.3)%、(72.5±3.4)%和(54.5±1.9)%.结论:RhoC/ROCK-Ⅰ信号转导通路与人卵巢癌细胞的体外侵袭与迁移密切相关,阻断ROCK-Ⅰ的表达可有效地抑制卵巢癌肿瘤细胞的体外侵袭能力.     

寡核苷酸阻断ROCK-1蛋白对人卵巢癌细胞恶性行为的影响

目的通过反义寡核苷酸(ASODN)对ROCK-1的特异性阻断,探讨ROCK-1蛋白在卵巢癌转移中的作用。方法将ROCK-1反义寡核苷酸(ASODN)以脂质体介导,转染人卵巢癌细胞系SW626和Caov-3细胞,采用逆转录聚合酶链反应(RT-PCR)与Western blot印迹法,检测转染前后ROCK-1蛋白的表达,Boyden小室观察ROCK-1 ASODN对SW626和Caov-3细胞侵袭及迁移能力的影响,采用二苯基溴化四氮唑蓝(MTT)比色法,测定转染前后细胞增殖及黏附能力的变化。结果转染ROCK-1 ASODN后,2株细胞内ROCK-1蛋白的表达明显减少,最大抑制率可达49.0%;细胞的侵袭能力受到明显抑制,10μmol/L组和20μmol/L组SW626细胞的侵袭能力分别为对照组的75.6%±3.8%和54.7%±2.9%,Caov-3细胞为68.8%±4.7%和50.0%±4.5%;转染2种浓度ASODN的SW626和Caov-3细胞的随机运动能力分别为对照组的80.0%±1.3%、63.7%±1.9%、72.0%±1.3%和55.9%±2.5%;定向运动能力分别为对照组的83.9%±1.4%、64.1%±1.3%、72.5%±3.4%和54.5%±1.9%。转染后2株细胞的体外黏附能力和增殖能力,均未显示出明显的变化。结论ROCK-1蛋白的表达与人卵巢癌细胞的体外侵袭和迁移密切相关,阻断ROCK-1的表达,可有效地抑制卵巢癌肿瘤细胞的转移。     

MicroRNA-150对上皮性卵巢癌细胞增殖、凋亡和侵袭转移能力的影响

目的 研究microRNA-150(miR-150)在人上皮性卵巢癌细胞中的表达情况,及其对人上皮性卵巢癌细胞增殖、凋亡和侵袭转移能力的影响。方法 通过荧光实时定量PCR(qRT-PCR)检测各处理组细胞中的miR-150表达水平;利用MTT法、流式细胞技术、Transwell法探究miR-150的表达对上皮性卵巢癌细胞增殖、凋亡及侵袭转移能力的影响。结果 与正常卵巢上皮细胞(T29)相比,上皮性卵巢癌细胞(A2780和OVCAR3)中miR-150表达显著降低(P＜0.01);转染miR-150mimic后,A2780和OVCAR3细胞中miR-150水平明显升高(P＜0.01);MTT试验显示,转染培养三天后,miR-150 mimic组细胞OD值(A2780:1.12±0.03;OVCAR3:1.91±0.03)较Blank组(A2780:2.35±0.09;OVCAR3:2.63±0.07)及miR-150 NC组(A2780:2.18±0.07;OVCAR3:2.43±0.11)明显降低(P＜0.01);细胞凋亡检测显示:miR-150 mimic组凋亡率(A2780:16.10±0.58%;OVCAR3:15.16±1.30%)较Blank组(A2780:10.07±0.66%;OVCAR3:3.81±0.24%)及miR-150 NC组(A2780:10.36±1.08%;OVCAR3:4.89±0.07%)明显升高(P＜0.01);Transwell试验显示:miR-150 mimic组穿膜细胞数(A2780:38.67±2.03;OVCAR3:28.67±2.03)较Blank组(A2780:76.30±7.45;OVCAR3:55.67±3.18)及miR-150 NC组(A2780:74.33±5.78;OVCAR3:56.33±3.84)明显减少(P＜0.01)。结论 miR-150在上皮性卵巢癌细胞中表达降低,可能是上皮性卵巢癌增殖、侵袭转移的机制之一;上调miR-150的表达可以抑制上皮性卵巢癌细胞增殖、促进细胞凋亡,并且降低上皮性卵巢癌细胞侵袭转移能力。     

Down-regulation of MT1-MMP expression suppresses tumor cell invasion in metastatic human SW626 ovarian cancer cells

Membrane-type 1 matrix metalloproteinase (MT1-MMP/MMP-14) is a key enzyme involved in degradation of extracellular matrix (ECM) and various surface-associated proteins that control cell growth, differentiation and survival, plays crucial roles in molecular carcinogenesis, tumor cell growth, invasion, and angiogenesis. We tested the inhibitory effect of antisense MT1-MMP on the ability of metastatic human ovarian carcinoma cell line SW626 in proliferation and invasion. RT-PCR was used to amplify MT1-MMP cDNA fragments with two different restriction sites at its 5'-end. Antisense MT1-MMP cloned in eukaryotic expression vector pMMP14as was transfected into SW626 cells. MT1-MMP protein expression, activities of MMP-2 and MMP-9, changes of cell proliferation, and cell invasion ability were detected by Western blot, optimized gelatin zymography, MTT assay and matrigel in vitro invasion assay, respectively. After 48 h transfection, decreased expression of endogenous MT1-MMP protein was detected in pMMP14as-transfected SW626 cells and showed significantly lower proliferation level when compared with control cells. The activation of proMMP-2 was inhibited markedly, and the mean percentage of invasive cells was 63.30+/-5.80% in pMMP14as-transfected cells, which was less than that (97.60+/-7.50%) in control cells (P<0.05). Both cell proliferation and invasion in SW626 cells were inhibited effectively by antisense MT1-MMP transfection, suggesting that MT1-MMP may be a proper target molecule for anti-invasion therapy for human ovarian cancers.     

慢病毒载体介导 CDK2 基因沉默对黑素瘤B16-F1细胞生物学行为的影响

目的:探讨由慢病毒载体pUL介导的pUL-CDK2-shRNA3 (CDK2-shRNA)沉默CDK2基因后对小鼠黑素瘤B16-F1细胞恶性生物学行为的影响,初步探索其作用机制.方法:利用重组慢病毒载体CDK2-shRNA转染B16-F1细胞,MTT法检测其对细胞增殖的影响,DAPI染色、AnnexinV-FITC/PI双染流式术检测细胞凋亡情况,流式术检测细胞周期变化,细胞黏附实验、transweU小室实验分别检测细胞黏附、侵袭和迁移能力变化,Western blotting检测细胞周期信号通路上RB蛋白(成视网膜细胞瘤蛋白)、pRB蛋白、细胞周期相关转录因子E2F1及侵袭迁移相关蛋白基质金属酶-2(MMP-2)、基质金属酶-9(MMP-9)的表达水平.结果:与空白对照组和阴性对照组相比,CDK2-shRNA组细胞相对增殖率、细胞黏附率、细胞侵袭和迁移能力均显著下降(均P＜0.05).细胞凋亡率显著增加(均P＜0.05);G1期细胞显著增加而S期和G2期显著降低(P＜0.05).细胞周期相关蛋白pRB、E2F1明显降低而RB显著升高(P＜0.05),细胞侵袭和迁移相关蛋白MMP-2、MMP-9明显降低(P＜0.05).结论:慢病毒载体pUL介导的shRNA沉默CDK2基因对B16-F1细胞恶性生物学行为有显著的抑制作用,其机制主要与细胞周期和细胞侵袭迁移相关蛋白表达变化有关.     

Adhesion induces matrix metalloproteinase-9 gene expression in ovarian cancer cells

The processes of cell invasion includes adhesion, proteolysis of extracellular matrix (ECM) and migration. It is not only related to cancer cells metastasis, but also involved in infiltration of immune effector cells,embryogenesis and angiogenesis. During the invasioncells attach and spread on the ECM, secrete proteinase to hydrolyze ECM, and then move through interstitial stroma. Matrix metalloproteinases (MMP), especially MMP-2 and MMP-9, play an important role in this processe[1,2].…     

基质金属蛋白酶-9反义寡核苷酸对卵巢癌细胞侵袭黏附能力的影响

目的 观察基质金属蛋白酶-9（MMP-9）反义寡核苷酸（ASODN）转染对卵巢癌细胞体外侵袭黏附行为的影响,并探讨其作用机制。方法 以Lipofectinmin介导的MMP-9反义寡核苷酸转染至经纤黏连蛋白诱导MMP-9表达的卵巢癌细胞株HO-8910PM,利用RT—PCR、Western blot及明胶酶谱法检测转染寡核苷酸后HO-8910PM细胞MMPO的mRNA、蛋白表达及酶活性的变化;通过细胞体外侵袭、迁移实验和黏附实验,检测细胞侵袭黏附能力的变化。结果 卵巢癌细胞HO-8910PM转染MMP-9反义寡核苷酸后,MMP-9的mRNA及蛋白的表达受到抑制,抑制率分别为34．8％和42．5％,与对照组比较,差异有统计学意义（P〈0．05）;明胶酶活性也受到了抑制。反义寡核苷酸的转染降低了肿瘤细胞体外侵袭、迁移和黏附能力,侵袭和迁移抑制率分别为22．4％和24．8％,在60min和90min黏附抑制率分别为49．8％和38．3％。结论 MMP-9反义寡核苷酸可抑制卵巢癌细胞的侵袭黏附能力,MMP-9有可能成为抗卵巢癌侵袭转移的分子靶点。     

PEBP4 enhanced HCC827 cell proliferation and invasion ability and inhibited apoptosis

The purposes of this study were to investigate the effects of phosphatidylethanolamine-binding protein 4 (PEBP4) on the cell growth, proliferation, apoptosis, and invasion of non-small cell lung cancer (NSCLC) cells and to provide evidence for future treatment options for NSCLC. Western blot assays were performed to examine PEBP4 protein expression levels in NSCLC cell lines (HCC827, A549, NCI-H661, NCI-H292, and 95-D) and a normal human bronchial epithelial (HBE) cell line. A PEBP4 shRNA expression vector was constructed and transfected into HCC827 cells. Subsequently, the effects of PEBP4 on the cell viability, cell cycle distribution, apoptosis levels, and invasion properties of HCC827 cells were analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, flow cytometry analyses, and transwell invasion assays. In addition, the effects of PEBP4 on the expression of proteins including cyclin D1, p53, Bcl-2, MMP-2, and MMP-9 were investigated. PEBP4 was highly expressed in lung cancer cells (HCC827, A549, NCI-H661, NCI-H292, and 95-D), but its expression was low in HBE cells. Cell viability, cell proliferation, and invasion of HCC827 cells in the PEBP4 knockdown group were significantly lower than that in the negative control and blank control groups (p?<?0.05), and there were no significant differences between the negative and blank control groups in terms of cell viability, cell proliferation, apoptosis, and invasion. In HCC827 cells, the expression levels of cyclin D1, Bcl-2, MMP-2, and MMP-9 in the PEBP4 knockdown group were significantly lower (p?<?0.05), and the expression of p53 protein was significantly higher than that in the negative and blank control groups (p?<?0.05). There were no significant differences between the negative and blank control groups in the expression levels of cyclin D1, p53, Bcl-2, MMP-2, and MMP-9. In conclusion, PEBP4 enhanced HCC827 cell proliferation and invasion ability and inhibited apoptosis. Decreased PEBP4 expression may play a role in the reduced invasion ability and increased apoptosis of the human NSCLC cell line HCC827.