microRNA-483在结肠癌细胞中的表达及临床意义

目的:检测结肠癌细胞系SW480及正常黏膜细胞中microRNA-483(miR-483)的差异表达,探索miR-483的表达对SW480细胞生长和耐药性的影响.方法:采用实时荧光定量PCR技术比较结肠癌细胞及正常黏膜细胞中miR-483的表达差异.通过MTT法及裸鼠成瘤实验探索miR-483对SW480细胞生长的调控作用.通过流式细胞仪检测阿霉素ADR诱导的SW480细胞凋亡.结果:miR-483在结肠癌细胞中的表达升高.下调miR-483不仅抑制SW480细胞的体内外增殖能力,还能增强SW480细胞的药物敏感性.结论:miR-483在结肠癌细胞中高表达,且在结肠癌细胞增殖和耐药中发挥调控作用.     

芹菜素对人结肠癌细胞SW480增殖抑制作用的实验研究

目的:观察芹菜素对体外培养的人结肠癌SW480细胞的增殖抑制作用.方法:观察不同浓度[(10、30、60、90)μmol/L]的芹菜素在(24、48、72)h对人结肠癌SW480细胞增殖的影响:光学显微镜和电子显微镜观察芹菜素处理后人结肠癌SW480细胞形态结构的变化;运用四唑盐比色法(MTY)检测芹菜素对人结肠癌SW480细胞生长的影响.结果:经芹菜素处理的人结肠癌SW480细胞数量减少,部分细胞体积缩小,细胞膜完整,胞浆浓缩,核染色质固缩,细胞核碎裂,形成凋亡小体;MTT法检测显示芹菜素对人结肠癌SW480细胞的增殖有抑制作用,其抑制作用随着作用浓度的增加和作用时间的延长而增强.结论:芹菜素对人结肠癌SW480细胞的增殖有抑制作用,是一种高效低毒的药物.     

丙氨酰谷氨酰胺对结肠癌细胞功能性FasL基因表达的影响

目的:研究丙氨酰谷氨酰胺(A1a-Gln)对人结肠癌SW480细胞FasL mRNA表达及其诱导淋巴细胞凋亡的影响,为进一步研究和应用谷氨酰胺提供依据.方法: 经体外培养结肠癌SW480细胞株,加入不同浓度的A1a-Gln后收集细胞.应用实时定量逆转录-聚合酶链反应(Real -Time RT-PCR)法检测人结肠癌SW480细胞FasL mRNA的变化;应用流式细胞术检测SW480细胞诱导淋巴细胞凋亡率的变化.结果: Real -Time RT-PCR法检测结果显示,不同浓度A1a-Gln处理后SW480细胞FasL mRNA表达水平均明显低于对照组(P<0.05);而且FasL mRNA表达水平随A1a-Gln作用浓度增加而下调,A1a-Gln不同浓度组比较均有显著性差异(P<0.05);流式细胞术检测结果表明,随A1a-Gln作用浓度升高,SW480细胞诱导淋巴细胞凋亡率降低,不同浓度组比较均有显著性差异(P<0.05).结论: 在一定浓度范围内,Ala-Gln可下调人结肠癌SW480细胞FasL mRNA的表达,并能抑制肿瘤细胞反向攻击淋巴细胞.     

DcR3-RNAi对人SW-480结肠癌细胞系恶性表型的影响

目的:观察研究抑制DcR3基因表达的人SW480结肠癌细胞其恶性表型的改变.方法:应用RNA干扰(RNAi)技术,构建小双链DNA,克隆入表达载体,转染进入SW480结肠癌细胞系(DcR3高表达细胞),在细胞内形成小干扰双链RNA;识别并降解DcR3 mRNA.筛选DcR3低表达转染癌细胞,3H观测其体外DcR3-SW480-RNAi转染细胞的增长率及凋亡表达.结果:转染的DcR3-SW480-RNAi-F1R1细胞可降低DcR3 mRNA的转录,凝胶电泳反应产物显示与对照组相比,DcR3-SW480-RN-Ai-F1R1细胞组条带明显减弱;3H掺入细胞的定量分析显示DcR3-RNAi-SW480结肠癌细胞的数量明显减少,P<0.001;Western 印记检测显示凋亡抗体Caspase-3及PARP表达增加.结论:经转染的DcR3-RNAi-SW480结肠癌细胞其DcR3 mRNA表达降低.肿瘤细胞的生长数量减少,凋亡表达增加, 有一定可探索性抗癌前景.     

结肠癌来源外泌体通过HMGB1诱导中性粒细胞活化促进结肠癌细胞增殖、侵袭和迁移

目的 探讨结肠癌细胞来源外泌体在中性粒细胞和结肠癌细胞间的作用及其可能的作用机制.方法 体外培养中性粒细胞和结肠癌细胞SW480,分别用sh?NC和sh?HMGB1转染SW480细胞后分离相应外泌体SW480?exo、sh?NC?exo、sh?HMGB1?exo.各组外泌体分别处理中性粒细胞,同时设置PBS组;提取各组...     

人结肠癌放射抗拒性细胞株的建立

目的应用连续照射的方法建立人结肠癌放射抗拒细胞株SW480-R,为研究人结肠癌放射抗拒的机制提供模型。方法用2Gv剂量的x射线照射人结肠癌SW480细胞株,每天1次,每周5d,分别照射不同周期后,按照细胞存活率筛选出放射抗拒细胞株SW480．R,并检测细胞的倍增时间。以细胞克隆形成实验检测细胞的放射敏感性,MTT法检测照射后不同时间点的细胞存活分数,流式细胞仪检测细胞的细胞周期分布,并分别与亲代结肠癌细胞株进行比较。结果经2Gy照射3周后细胞仍有存活,可作为放射抗拒细胞株的模型。SW480．R细胞株的倍增时间明显长于亲代SW480细胞株（脚．05）,SW480-R细胞株的放射抗拒l生增加,照射后12h的细胞存活率较SW480细胞株显著增高（98．40％US92．81％,P〈0．001）。流式细胞仪检测细胞周期显示,SW480一R细胞株的细胞周期分布与SW480细胞株不同,G2／M期明显增高。结论人结肠癌细胞株SW480每天经x射线照射2Gy,连续照射3周后可以得到具有放射抗拒细胞株SW480．R。此细胞株具有稳定的放射抗拒性,且与亲代细胞株有不同的细胞周期分布。     

TRPV5 TRPV6对结肠癌SW480细胞生物学行为的影响

  目的  观察TRPV5和TRPV6蛋白表达水平对结肠癌SW480细胞内Ca2+水平及细胞增殖、凋亡、迁移等生物学行为的影响。  方法  给予TRPV5、TRPV6通道激动剂1-25（OH）₂D₃及抑制剂CuCl₂作用结肠癌SW480细胞后,采用免疫组织化学法、Western blot及实时荧光定量PCR技术检测TRPV5、TRPV6蛋白及TRPV5、TRPV6 mRNA表达的变化。使用高速离子成像系统观察结肠癌SW480细胞内Ca2+水平的变化;通过MTT法、TUNEL法及划痕修复法观察结肠癌SW480细胞增殖凋亡及迁移的变化。  结果  1-25（OH）₂D₃明显上调结肠癌SW480细胞TRPV5、TRPV6 mRNA及蛋白表达水平,使结肠癌SW480细胞内Ca2+水平增加,促进结肠癌SW480细胞增殖、迁移及抑制其凋亡（P＜0.05）。CuCl₂明显下调结肠癌SW480细胞中TRPV5、TRPV6蛋白及mRNA表达,使结肠癌SW480细胞内Ca2+水平降低（P＜0.05）,抑制结肠癌SW480细胞的增殖、迁移及促进细胞的凋亡（P＜0.05）。  结论  结肠癌SW480细胞中TRPV5和TRPV6蛋白表达水平的变化,能通过调控细胞内Ca2+水平影响细胞的增殖、迁移和凋亡等生物学行为。      

干扰素诱导跨膜蛋白1协同干扰素抑制结肠癌细胞增殖

目的：研究干扰素诱导跨膜蛋白1(interferon induced transmembrane protein 1,IFITM1)协同干扰素对结肠癌细胞株SW480增殖的影响。方法：将IFITM1基因亚克隆到真核表达载体pEGFP-C3,IFITM1/pEGFP-C3重组质粒转染结肠癌细胞株SW480,G418 500mg/L筛选阳性克隆细胞。激光共聚焦显微镜及RT-PCR检测IFITM1的表达。实验设pEGFP- C3/SW 480组、IFITM1/SW 480组、IFITM1/anti-IFITM1/SW 480、空白组,除空白组外,每组加入IFN_(-α) 1000 U/mL。MTT检测细胞的增殖性。结果：IFITM1/pEGFP-C3重组质粒转染SW480细胞后,激光共聚焦显微镜观察到绿色荧光融合蛋白位于细胞膜周围,RT-PCR在IFITM1/SW 480细胞中检测到IFITM1 mRNA表达,SW 480细胞及pEGFP-C3/SW480细胞中未见IFITM1 mRNA表达。MTT分析细胞增殖示pEGFP-C3/SW 480组、IFITM1/SW 480组、IFITM1/anti-IFITM1/SW 480组的D_(570mm)处值分别0.745±0.0267、0.346±0.0316、0.696±0.0613,空白组的D_(570mm)值是0.835±0.0362,IFITM1/SW 480细胞增殖比pEGFP-C3/SW 480细胞及IFITM1/anti-IFITM1/SW 480细胞低(P＜0.05)。而pEGFP-C3/SW 480细胞的增殖与IFITM1/anti-IFITM1/SW 480细胞增殖相比无显著差异(P＞0.05)。结论：IFITM1可协同IFN-α抑制SW 480细胞体外增殖。     

p33ING1b基因对人结肠癌细胞SW480生物学行为的影响

目的:构建pcDNA3.1( )/p33ING1b真核表达载体及观察其对人结肠癌细胞SW480生长的影响。方法:构建人p33ING1b真核表达载体,采用脂质体转染方法,将pcDNA3.1( )/p33ING1b转染人结肠癌细胞系SW480,G418筛选,挑选阳性克隆,阳性克隆经RTPCR及Westernblot鉴定后,通过生长曲线和软琼脂克隆形成实验检测高表达p33ING1b基因的SW480细胞体外增殖情况,并用流式细胞仪分析细胞凋亡率的改变。结果:成功构建重组pcDNA3.1( )/p33ING1b基因的真核表达载体,建立高表达p33ING1b基因的SW480细胞系,p33ING1b基因在SW480细胞中高表达后,其生长速度减慢,细胞凋亡率(15.4±1.7)%较空载体组(2.0±0.6)%及未转染组(1.6±0.8)%明显升高。结论:p33ING1b基因高表达对SW480细胞系具有生长抑制和促进凋亡的作用。     

中药夏枯草对结肠癌细胞FasL基因表达和侵袭能力的影响

目的:研究夏枯草对人结肠癌SW480细胞FasLmRNA表达及对其侵袭能力的影响,为中药抗肿瘤提供实验依据.方法: 根据MTT法得到夏枯草对SW480细胞的半数有效抑制浓度(IC50),确定药物作用浓度.SW480细胞分别经夏枯草不同浓度(0.5IC50、IC50)作用后,应用逆转录-聚合酶链反应(RT-PCR)法检测夏枯草作用前后人结肠癌SW480细胞FasL mRNA的变化;应用Transwell细胞侵袭试验检测夏枯草对SW480细胞侵袭能力的影响.结果: 夏枯草处理后较处理前SW480细胞FasL mRNA表达水平均明显高于对照组(P<0.01);而且FasL mRNA表达水平随夏枯草作用浓度增加显著上调,夏枯草不同浓度组比较均有显著性差异(P<0.01);随夏枯草作用浓度升高,SW480细胞侵袭能力明显增强,不同浓度组比较均有显著性差异(P<0.01).结论: 夏枯草在一定时间内均可上调人结肠癌SW480细胞FasL mRNA的表达,而且这种上调作用在一定范围内呈剂量依赖性,可使结肠癌细胞的侵袭能力增强.     

Let-7b-5p inhibits colon cancer progression by prohibiting APC ubiquitination degradation and the Wnt pathway by targeting NKD1

Naked cuticle homolog 1 (NKD1), which is expressed at low levels in many tumors, is considered an inhibitor of the Wnt/β-catenin pathway, but it is highly expressed in colon cancer and can promote colon cancer cell proliferation. miRNAs are involved in the occurrence and progression of many tumors. However, miRNAs that can regulate NKD1 and the mechanisms by which NKD1 regulates tumor progression remain ambiguous. This research aims to reveal the potential regulatory network of NKD1 in colon cancer. miRNA data downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were analyzed by bioinformatics to screen for potential miRNAs targeting NKD1. Let-7b-5p was found to inhibit proliferation, migration, and invasion of colon cancer cells targeting NKD1. Further studies suggested that let-7b-5p can modulate Wnt signaling activity, and the nuclear accumulation of β-catenin was significantly restrained by let-7b-5p through targeting NKD1. Moreover, NKD1 could prohibit the expression of the APC protein. Further studies manifested that NKD1 bound to APC and promoted the ubiquitination degradation of APC through restraining the expression of the deubiquitinating enzyme USP15 and blocking the combination between USP15 and APC. Functionally, NKD1 enhanced the proliferation and migration of colon cancer cells by inhibiting APC expression. This research revealed a novel mechanism by which the let-7b-5p-NKD1-APC-β-catenin signaling pathway inhibited colon cancer cell progression.     

Axin通过激活p53的表达抑制结肠癌细胞的生长

目的： 观察过表达Axin对结肠癌SW480细胞生长的影响,并探讨其作用机制。方法：将pCMV5-HA-Axin质粒瞬时转染至结肠癌SW480细胞中,并设置转染空载体pCMV5-HA及未转染空白对照组,采用噻唑蓝(MTT)比色法及克隆形成实验检测细胞增殖状态的变化,流式细胞仪检测细胞周期变化;RT-PCR检测Axin及p53 mRNA的表达;Western blot检测Axin及P53蛋白的表达。结果：与转染空载体及空白对照组比较,过表达Axin显著抑制结肠癌SW480细胞的增殖。MTT实验显示转染Axin后细胞生长明显受到抑制,存活的瘤细胞明显减少(P<0.05);克隆形成实验结果显示瞬时转染Axin质粒组细胞集落形成能力明显下降(P<0.05);流式细胞仪分析检测结果显示转染Axin质粒后结肠癌SW480细胞周期G1前期比例升高,G1期明显被阻滞,S期比例下降(P均<0.05)。RT-PCR结果显示转染Axin的SW480细胞中p53 mRNA的表达较转染空载体组升高约1倍(P＜0.05);同时,Western blot结果显示转染质粒Axin后结肠癌SW480细胞中P53的蛋白表达量明显增加,较转染空载体组几近升高1倍(P＜0.05)。结论：过表达Axin抑制结肠癌SW480细胞增殖,其作用机制是通过激活癌基因p53的表达而发挥效应的。     

Modulation of POPDC1 Expression by Phenothiazine and Trifluoperazine Suppress Colon Cancer Growth and Migration

Objective: The aim of this study was to investigate the effects of CaM antagonist, PTZ, and TFP on cell proliferation and migration of colon cancer cells and its impact on POPDC protein expression. Methods: The 50% inhibitory concentration (IC50) of PTZ and TFP in SW1116, SW480, HCT-15, and COLO205 colon cancer cell lines are measured using MTT. Western blot and immunocytochemistry were used to determine the expression of PCNA, cyclin D1 (CD1), and POPDC proteins. Cell migration was observed using a scratch wound-healing assay. Results: Treatment with PTZ and TFP inhibited colon cancer cells growth in a dose-dependent manner. PTZ and TFP significantly inhibited the activation of proliferation markers, PCNA and CD1, and the migration of colon cancer cells. Furthermore, POPDC protein was significantly suppressed in all cell types of colon cancer, particularly in SW480. Finally, the CaM antagonist upregulates the POPDC1 expression in colon cancer cells. Conclusion: These findings suggest that CaM antagonists suppress colon cancer cells proliferation via downregulation of CD1 and PCNA. In addition, POPDC protein could be used as a biomarker in colon cancer, and CaM antagonist could be used to regulate POPDC1 expression. This study suggests that targeting POPDC1 with CaM inhibition could be a potential therapeutic strategy for colon cancer treatment.     

Molecular cloning, gene structure, and expression analyses of NKD1 and NKD2

Mouse Nkd is a Dishevelled-binding protein, functioning as a negative regulator of WNT - beta-catenin - TCF signaling pathway. Here, human NKD1 and NKD2 were cloned and characterized. NKD1 and NKD2 were predicted to encode 470- and 451-amino-acid polypeptide, respectively. NKD1 and NKD2, showing 43.8% total amino-acid identity, were more homologous in the NH1, NH2, NH3, and NH4 domains. The NH2 domain of NKD1 and NKD2 contained the EF-hand motif. Exon-intron structures of NKD1 and NKD2 genes, consisting of 10 exons, were well conserved. NKD1 was highly expressed in fetal kidney, while NKD2 was moderately expressed in fetal kidney, lung, and adult lung. NKD1 was up-regulated in colorectal cancer cell line SW480, gastric cancer cell line TMK1, and pancreatic cancer cell line Hs700T. NKD2 was up-regulated in gastric cancer cell line MKN45, pancreatic cancer cell line BxPC-3, and esophageal cancer cell lines TE6, and TE13. NKD1 and NKD2 were up-regulated together in 1 case of primary gastric cancer out of 10 cases, and were down-regulated together in 2 cases. Up-regulation of NKD1 or NKD2 might be due to a negative feed-back mechanism. Alternatively, genetic alteration of NKD1 or NKD2 might lead to activation of the WNT - beta-catenin - TCF signaling pathway.     

YAP蛋白在结肠癌中的表达及其对SW480细胞增殖和侵袭的影响

目的:研究YAP蛋白在结肠癌中的表达及临床意义, 并初步探讨其对结肠癌细胞增殖、侵袭的影响。方法:免疫组化检测YAP蛋白在25例结肠癌组织及配对正常组织中的表达,并分析其与结肠癌临床病理特征之间的关系;用Real-Time PCR和 Western blot验证YAP-shRNA慢病毒载体转染效率;生长曲线实验和MTT法检测下调YAP表达对结肠癌细胞SW480增殖的影响;Transwell实验检测下调YAP表达对结肠癌细胞SW480侵袭的影响;Western blot检测下调YAP表达对CyclinD1、E-cadherin及Vimentin蛋白的影响。结果:YAP在结肠癌组织中的表达显著高于正常结肠组织（P＜0.05）,并且与淋巴结转移密切相关(P＜0.05);转染YAP-shRNA慢病毒载体的SW480细胞YAP的表达在mRNA 和蛋白水平明显降低（均P＜0.05）;下调YAP表达后结肠癌细胞增殖及侵袭明显减弱（均P＜0.05）;下调YAP 表达可抑制结肠癌细胞CyclinD1、E-cadherin及Vimentin蛋白的表达（均P＜0.05）。结论:YAP在结肠癌组织中高表达,且与淋巴结转移相关,下调YAP表达可抑制结肠癌细胞增殖及侵袭能力,预示YAP在结肠癌恶性进展中具有重要的作用。     

外源人核受体hLRH-1在结肠腺癌细胞SW480中表达的生物学效应及其分子机理初探

Objective： To explore the possible biological function of human nuclear receptor hLRH-1 in tumorigenesis and progress of colon cancer. Methods： Plasmids pcDNA3-hLRH-1 were introduced into SW480 cells via lipofectamine. The expression of mRNA and protein of exogenous hLRH-1 were detected by RT-PCR and western blotting, respectively. MTT assay was carried out to survey the proliferation of SW480 cells with overexpression of hLRH-1. Meanwhile, the expression of proliferation-related genes cyclin E1 and cyclin D1, and apoptosis-related genes PTEN and Rbl, were analyzed by realtime RT-PCR. Results： The proliferation of SW480 cells was promoted under the condition of overexpression of hLRH-1. The expression of cyclin E1 was up-regulated significantly, while that of PTEN and Rbl were down-regulated in SW480 cells with overexpressed hLRH-1. Conclusion： The expression of exogenous hLRH-1 in SW480 cells induced the proliferation resulting form up-regulation of cyclin E1, as well as participated in the regulation of apoptosis via influencing the expression of PTEN and Rb1.     

结肠癌细胞通过Fas/FasL诱导淋巴细胞发生凋亡

背景与目的:研究发现,肿瘤组织中Fas配体阳性表达区肿瘤浸润淋巴细胞的凋亡率比FasL阴性区高,推测肿瘤细胞可通过增加表达FasL来杀伤肿瘤浸润淋巴细胞。本研究拟在体外验证结肠癌细胞SW480是否可以诱导淋巴细胞发生凋亡。方法:结肠癌细胞系SW480(效应细胞)与对Fas介导凋亡敏感的Jurkat细胞(靶细胞)共培养,分为3种效靶比20∶1,10∶1,5∶1。生长曲线法、流式细胞术、荧光显微镜观察分别检测Jurkat细胞的凋亡情况。结果:流式细胞仪检测结果显示,SW480接种浓度为0(对照)、0.5×105/ml、1×105/ml、2×105/ml时,Jurkat细胞凋亡率为(1.8±0.21)%、(5.49±0.17)%、(11.18±0.14)%、(18.22±0.11)%。荧光显微镜观察结果表明,SW480接种浓度为0(对照)、0.5×105/ml、1×105/ml、2×105/ml时,Jurkat细胞凋亡率为(1.58±0.12)%、(5.22±0.13)%、(9.74±0.21)%、(19.33±0.18)%。3种效靶比条件下,SW480细胞均能诱导Jurkat细胞发生凋亡。随着SW480接种浓度的升高及共培养作用时间的延长,Jurkat细胞凋亡率逐渐增加。每个实验组与对照组相比,P值均小于0.01。结论:结肠癌细胞SW480可以通过Fas系统诱导淋巴细胞发生凋亡,这为结肠癌的免疫逃逸、反击机制提供了又一证据。     

上调结肠癌间充质干细胞中miR-93-5p表达抑制结肠癌细胞增殖及促进凋亡的机制探讨

目的:观察miR-93-5p上调的结肠癌间充质干细胞（colon cancer mesenchymal stem cell,CCMSC）对结肠癌细胞增殖、凋亡的影响,并初步探讨其机制。方法:以贴壁细胞培养法抽提癌组织CCMSC,从正常结肠组织抽提结肠间充质干细胞（colon mesenchymal stem cell,CMSC）,观察miR-93-5p及PD-L1的表达差异;以拟似剂上调CCMSC中miR-93-5p表达,CCK8法及流式细胞术检测CCMSC诱导的SW480细胞增殖及凋亡变化。结果:miR-93-5p在结肠癌细胞株中表达低于正常结肠上皮细胞（P＜0.001）,PD-L1 mRNA和PD-L1蛋白在结肠癌细胞株中表达高于正常结肠上皮细胞（P＜0.001,P＜0.001）;miR-93-5p在CCMSC组中表达明显低于CMSC（P＜0.001）;与SW480细胞比较,给予CCMSC干预后SW480细胞存活率上升（P＜0.001）,凋亡率下降（P＜0.05）,与SW480细胞或CCMSC/SW480细胞比较,给予转染miR-93-5p mimics CCMSC干预的SW480细胞存活率下降（P＜0.01,P＜0.001）,凋亡率上升（P＜0.05,P＜0.01）。结论:上调CCMSC中miR-93-5p通过靶向调控PD-L1抑制结肠癌细胞增殖,促进凋亡。     

p53 dependence and apoptosis in response to FP treatment with p53-transfected colon cancer cell lines by use of thin layer collagen gel

The combination of 5-fluorouracil (5-FU) plus Cisplatin (CDDP) (FP treatment) possesses synergistic cytotoxicity against colon cancer. The molecular mechanisms by which chemotherapeutic agents induce apoptosis have been clarified by identifying apoptosis-related genes such p53 and bcl-2. We previously established a new experimental technique in which cancer cells are distributed in thin collagen gel as 1 or 2 cell layers. additionally, we evaluated the efficacy and toxicity of FP treatment in the gastric and colon cancer cell lines, and examined the relationship between the response to FP treatment and apoptosis. In these results we reported transfection of normal p53 gene into p53 mutant and analyzed the impact of the p53 gene in a sensitivity test. In this study, we examined induced apoptosis in colon cancer cell lines and the status of p53 expression in response to treatment of HCT116, COLO320, SW480 and DLD1 with 5-FU alone, CDDP alone and FP treatment under flow cytometric analysis. Transfection of SW480 and DLD1 cells was performed to compare the chemosensitivity of naturally occurring mutant-type p53 SW480 and DLD1 cells with neo-transfected SW480 and DLD1 cells and transfected SW480 and DLD1 cells. Appreciable apoptosis was induced in HCT116 and COLO320 (p53 wild-type) but not in SW480 and DLD1 cells (p53 mutant-type). Transfected SW480 and DLD1 cells underwent significantly more apoptosis (p相似文献