小片段RNA干扰提高人卵巢癌耐药细胞对化疗药物的敏感性研究

目的采用针对多药耐药基因MDR1的小片段RNA(siRNA)转染人卵巢癌耐药细胞株,了解转染后能否提高细胞对化疗药物的敏感性。方法用脂质体将合成针对MDR1的siRNA转染具有MDR1高表达的人卵巢癌泰素耐药细胞株OVCAR8/TR,并用ATP生物发光法检测转染前、后细胞对顺铂、5-氟脲嘧啶、阿霉素和泰素4种化疗药物敏感性的变化。结果OVCAR8/TR细胞对顺铂、阿霉素和泰素均耐药,转染后细胞能够明显提高通过P-gp转运药物泰素和阿霉素的敏感性,泰素对细胞的抑制率由转染前的26%提高到78%,阿霉素对细胞的抑制率则由转染前的37%提高到58%,对顺铂的耐药性则没有改变。单用脂质体转染组的药敏结果与未转染组差异无统计学意义。结论siRNA干扰能够逆转人卵巢癌化疗药物的多药耐药,提高对化疗药物的敏感性。     

靶向MDR1基因siRNA逆转HepG2/ADM细胞耐药性的研究

目的 采用RNA干扰技术逆转人类肝癌细胞系/阿霉素(human hepatocellular liver carcinoma cell line/adriamycin,HepG2/ADM)细胞中多耐药基因,探讨该基因能否有效地抑制多耐药基因(multidrug resistance gene,MDR1)及其编码的糖蛋白(P-glycoprotein,P-gp)的表达,并检测对HepG2/ADM耐药表型的逆转效果.方法 采用药物大剂量冲击法建立HepG2/ADM耐药模型,构建靶向MDR1的小干扰RNA表达载体,并转染到HepG2/ADM细胞中,应用半定量逆转录-聚合酶链反应检测基因转染前后MDR1 mRNA表达水平的变化,Western-blot检测各组细胞P-gp蛋白表达的变化,用噻唑蓝法检测各组细胞对阿霉素、顺铂、长春新碱和氟尿嘧啶等药物的敏感性.结果 HepG2/ADM细胞系不仅对阿霉素耐药,而且对其他化疗药也有抗性,呈现多药耐药特性;重组质粒鉴定结果表明针对MDR1的小干扰RNA表达载体成功构建;与对照组比较,转入细胞后MDR1 mRNA水平明显下降,P-gp蛋白表达明显降低;转入细胞后HepG2/ADM细胞对化疗药物的敏感性明显提高,部分逆转其耐药性.结论 靶向MDR1的小干扰RNA可显著抑制HepG2/ADM细胞中MDR1基因和P-gp蛋白的表达,逆转P-gp介导的HepG2/ADM细胞的耐药性.     

抑制P-糖蛋白表达逆转视网膜母细胞瘤多药耐药研究

目的:探讨应用RNA干扰(RNAi)技术逆转视网膜母细胞瘤多药耐药的可行性。方法:将设计合成的针对多药耐药基因MDR1的特异性小分子干扰RNA(siRNA),用脂质体转染具有MDR1基因高表达的视网膜母细胞瘤耐药细胞株SO-Rb50/VCR。用实时定量RT-PCR技术和Westernblot分别测定转染前后细胞MDR1mRNA及P-糖蛋白(P-gp)表达的变化;用CCK-8法和TUNEL法检测转染前细胞株(VCR组),转染后细胞(VCR+siRNA组)对不同浓度长春新碱、依托泊苷和卡铂药物敏感性。结果:VCR+siRNA组较VCR组比较,MDR1基因在mRNA水平和蛋白水平表达显著下降,差异具有统计学意义。随着长春新碱、依托泊苷浓度的升高VCR+siRNA组较VCR组比较,细胞存活率显著降低,差异具有统计学意义。不同浓度的卡铂作用于VCR组、CT组和VCR+siRNA组细胞存活率、细胞凋亡率各组见未见显著性差异。随着长春新碱、依托泊苷浓度的升高,VCR+siRNA组较VCR组比较,细胞凋亡率显著性升高,差异具有统计学意义。结论:在SO-Rb50/VCR细胞中,针对MDR1合成的siRNA能够有效地抑制MDR1mRNA和P-gp的表达,并能恢复肿瘤细胞对长春新碱和依托泊苷的敏感性。应用RNAi技术,能够逆转Pgp引起的视网膜母细胞瘤多药耐药性。     

两种siRNA转染方法对T24/ADM多药耐药性的影响

目的:评价2种转染小干扰RNA(siRNA,small interfering RNA)方法对膀胱癌多药耐药性(MDR)的影响。方法:设计MDR基因的siRNA,用脂质体和电转的方法转染膀胱癌T24/ADM细胞,用RT-PCR分析mRNA的表达,流式细胞仪检测细胞内糖蛋白(P-gp)的表达和阿霉素积累量。结果:siRNA能明显地逆转T24/ADM细胞的多药耐药。电转染的方法抑制基因的效果优于脂质体转染的方法,P-gp表达下调,细胞内阿霉素积累量显著增加(P<0.05)。结论:2种转染方法均能够逆转膀胱癌的多药耐药性,电转染的方法优于化学转染方法。     

肿瘤细胞特异启动子hTERT介导的靶向mdr1基因的RNAi用于逆转卵巢癌细胞MDR的研究

目的:探索应用肿瘤细胞特异启动子hTERT介导靶向肿瘤多药耐药基因mdr1的siRNA在卵巢肿瘤细胞特异表达并逆转MDR的可行性。方法:应用携带luc报告基因的报告质粒验证了hTERT启动子在卵巢肿瘤细胞株A2780中的转录活性,构建由hTERT启动子引导的靶向mdr1基因的siRNA表达载体phTERTsiMDR1B,并与携带mdr1基因靶序列的报告质粒进行共转染抑制实验,进一步将phTERT-siMDR1B表达载体与mdr1基因表达载体共转染A2780细胞,检测细胞中mdr1基因的mRNA与P-gp蛋白的表达水平。以具有耐紫杉醇表型的A2780细胞作为靶细胞进行耐药评价实验。结果:hTERT启动子在卵巢肿瘤细胞株A2780中具有良好的转录活性,而在正常人二倍体细胞株MRC-5中无转录活性;hTERT启动子介导的siMDR1B具有良好的抑制效果与特异性;hTERT启动子介导的siMDR1B可显著抑制细胞中mdr1基因的mRNA与P-gp蛋白的表达水平;转染了hTERT启动子介导的siMDR1B表达元件的细胞对紫杉醇的耐药程度显著降低。结论:hTERT启动子介导的靶向mdr1基因的RNAi用于逆转卵巢癌细胞MDR是可行的,本研究结果可为进一步开展卵巢肿瘤MDR逆转研究提供重要基础。     

Reversal of multidrug resistance in renal cell carcinoma by short hairpin RNA targeting MDR1 gene

目的 研究RNA干扰（RNA interference,RNAi）对肾癌细胞多药耐药基因(MDRl)表达的抑制作用,并分析干扰前后肾癌细胞对化疗药物敏感性的变化。方法 根据MDRl基因设计3条小干扰RNA（small interfering RNA,siRNA）序列,在质粒的介导下转染肾癌A498细胞,RT-PCR法分析转染前后MDR1 mRNA表达水平,筛选出干扰效率最高的siRNA序列;进而利用慢病毒包装siRNA重组质粒,感染A498细胞,RT-PCR法筛选沉默效果最好的细胞株进行克隆,Western bolt法检测MDR1蛋白表达水平,MTT法对比干扰前后多种化疗药物对细胞半抑制浓度（IC50）的变化;相关数据统计通过SPSS10.0软件进行。结果 3条siRNA序列均能不同程度地抑制细胞MDR1基因的表达,其中siRNA-1序列能更有效地封闭MDRl基因,使MDRl mRNA表达水平下降;筛选出的稳转细胞株与未干扰细胞株相比,MDR1蛋白表达量明显下降,并使多种化疗药物对细胞的IC50明显降低。结论 RNAi技术可有效抑制肾癌A498细胞MDRl基因的表达,并可显著增加其对多种化疗药物的敏感性,从而使肾癌细胞化疗耐药逆转成为可能。     

siRNA逆转survivin介导的T24/AMD细胞多药耐药的研究

目的:研究siRNA(small interfering RNA)逆转survivin介导的膀胱癌多药耐药性。方法:设计针对survivin基因的siRNA,转染膀胱癌T24/ADM细胞,采用RT-PCR检测mRNA表达,免疫印迹法检测蛋白表达,流式细胞仪检测细胞内阿霉素累积量。结果:siRNA能明显逆转T24/ADM细胞的多药耐药,使survivin基因的mRNA及蛋白表达水平下调,细胞内阿霉素累积量显著增加(P<0.05)。结论:siRNA通过抑制survivin基因表达从而逆转膀胱癌的多药耐药。     

靶向葡萄糖神经酰胺合成酶逆转乳腺癌多药耐药的研究

目的:探讨靶向葡萄糖神经酰胺合成酶(glucosylceramide synthase,GCS)对乳腺癌多药耐药的逆转作用及机制。方法:GCS反义寡核苷酸(GCSASODN)转染人耐药乳腺癌细胞MCF-7/AdrR,RT-PCR检测细胞GCS和多药耐药基因1(MDR1)mRNA的表达,免疫细胞化学染色检测细胞GCS蛋白和P-糖蛋白(P-gp)的表达,流式细胞仪分析细胞周期和凋亡。Caspase-3活性测定法检测Caspase-3活性改变。结果:GCSASODN转染人耐药乳腺癌细胞MCF-7/AdrR后,GCS和MDR1mRNA的表达水平分别为0.3、0.7,GCS蛋白和P-gp表达阳性率分别为23%、33%,GCS和MDR1的mRNA和蛋白水平较对照组有显著性差异(P<0.05)。转染后细胞周期改变不明显,但细胞凋亡增加为13.7±4.1,Caspase-3活性升高为0.0725±0.0003,与对照组差异有显著性(P<0.01)。结论:靶向GCS通过直接抑制GCS活性,并间接下调MDR1mRNA和蛋白表达,激活Caspase-3活性,诱导耐药细胞凋亡增加,有效逆转乳腺癌多药耐药。     

短发夹RNA／MDR1逆转肝细胞癌多药耐药

有关RNA干扰（RNAi）逆转肿瘤多药耐药的实验研究报道较多,但绝大多数为细胞水平的体外实验。有报道将小RNA（siRNA）直接体内注射成功抑制目的基因表达…,但由于siRNA的不稳定性以及直接注射后的表达效率低下等问题,其可靠性值得商讨。我们在体外研究的基础上,探讨多药耐药基因（MDRI）的dsRNA质粒表达载体（PSUPER—shR-NA／MDR1）体内转染抑制多药耐药基因MDR1／p—gp表达的可能性。     

RNA干扰逆转肝细胞癌多药耐药

目的 筛选高效dsRNA/mdr1,以备研究RNA干扰逆转肝细胞癌多药耐药之用.方法 首先根据siRNA设计原则,以多药耐药基因(mdr1)为靶基因,设计并选择4～5条siRNA/mdr1,经BLAST后体外转录法合成dsRNA/mdr1,用Oligofectamine试剂分别转染HepG2/mdr1,然后从mRNA、蛋白(P-gp)表达水平和细胞功能变化评价HepG2/mdr1耐药性被逆转的程度,比较各个dsRNA/mdr1的逆转效率,筛选出有效的siRNA/mdr1.结果 成功合成5条dsRNA/mdr1(其中1条为阴性对照),dsRNA/mdr1-4 mRNA表达(18.73±1.33)%、蛋白表达变化(79.1±1.6)%～(16.8±0.4)%与其他各组细胞比较,有显著性差异;细胞内柔红霉素(DNR)累积量也较其他组明显增加(平均荧光强度79.58,阳性率84.25%,P＜0.05).结论 体外转录法结合脂质体转染适用于筛选高效siRNA,肯定了siRNA干扰序列能够有效阻抑mdr1基因编码蛋白p170的功能.     

MDR1 siRNA对结肠癌细胞多药耐药性的影响

 [目的]探讨MDR1 siRNA对结肠癌细胞多药耐药性的影响。[方法]设计合成两种针对MDR1 mRNA的siRNA双链分子（#4123 MDR1 siRNA和#4029 MDR1 siRNA）,并转染入COLO 320DM和HT-29结肠癌细胞,观察其对结肠癌细胞MDR1 mRNA和P-gp表达的影响。并分别与5-FU、阿霉素和长春新碱等抗肿瘤药联用,观察结肠癌细胞活力的变化。用阿霉素处理后,观察转染MDR1 siRNA结肠癌细胞的细胞内阿霉素累积浓度的变化。RT-PCR检测细胞MDR1 mRNA的表达,免疫印迹法检测细胞P-gp的表达,MTT法检测细胞活力,流式细胞术检测细胞内阿霉素累积浓度。[结果]#4123 MDR1 siRNA和#4029 MDR1 siRNA均可抑制COLO 320DM结肠癌细胞MDR1 mRNA和P-gp的表达,其最低有效浓度分别为5nmol/L和25nmol/L。同时MDR1 mRNA和P-gp表达的抑制伴随着抗肿瘤药（5-FU、阿霉素和长春新碱）对COLO 320DM结肠癌细胞毒性的增强和细胞内阿霉素累积浓度的增加。而在对照HT-29结肠癌细胞却观察不到此效应。[结论]MDR1 siRNAs能特异逆转结肠癌细胞的多药耐药性,为MDR1/P-gp依赖的多药耐药性结肠癌的治疗提供了一条新的途径。     

MDR1 and MDR3 Genes and Drug Resistance to Cisplatin of Ovarian Cancer Cells

To investigate the relationship between MDR1 and MDR3 gene and drug resistance to cisplatin of ovarian cancer cells. Two siRNAs (MDR1, MDR3) which specifically targeted MDR1 and MDR3 genes were transfered into A2780/DDP cells. Then double staining with Annexin- V-FITC/PI was used to detect cell apoptosis by the flow cytometry (FCM). A2780/DDP cell viability was determined by MTT. MDR1 and MDR3 mRNA were assessed by RT-PCR. Caspase-3 protein was detected by Western blotting. Transfection of MDR1 and MDR3 siRNA into A2780/DDP cells failed to reverse the drug-resistance of A2780/DDP cells to cisplatin (P>0.05). No significant differ- ence in the apoptosis efficiency was observed between the MDR1 and MDR3 siRNA, pSuppressor- Neo vector transfection cells and untreated cells (P>0.05). In the presence of cisplatin of different concentrations, the viability of A2780/DDP cells was not significantly decreased after the transfection. No changes in MDR1 and MDR3 mRNA were found in MDR1 and MDR3 siRNA-transfected A2780/DDP cells. As compared with pSuppressorNeo and untreated groups, no significant difference existed in the expression of MDR1 and MDR3 mRNA (P>0.05). The expression of caspase-3 protein in MDR1 and MDR3 siRNA transfected A2780/DDP cells was not significantly increased. It is con- cluded that multidrug resistance induced by cisplatin in ovarian carcinoma cell lines is not due to overexpression of MDR1 and MDR3 gene. The drug resistance of ovarian carcinoma cells to cisplatin is not mediated by P-glycoprotein.     

缺氧诱导因子-1α基因沉默逆转卵巢癌细胞SKOV3/DDP耐药性的机制

目的：观察缺氧诱导因子-1α(HIF-1α)沉默后人卵巢癌细胞顺铂耐药株SKOV3/DDP 的HIF-1α、多药耐药基因1 （MDR1）和B细胞淋巴瘤/白血病-2基因（Bcl-2）mRNA及蛋白产物的表达,探讨HIF-1α逆转SKOV3/DDP耐药性的机制。方法：体外培养卵巢癌细胞株SKOV3（敏感组）及其顺铂耐药株SKOV3/DDP（耐药组）,部分耐药株转染HIF-1α干扰质粒 pshRNA-HIF（转染组）及对照质粒pshRNA-Control（对照组）。RT-PCR法检测各组细胞HIF-1α、MDR1和Bcl-2 mRNA表达量;Western blotting和免疫组织化学法测定HIF-1α、P-gp（MDR1基因编码蛋白）和Bcl-2蛋白的表达量。结果：RT-PCR检测,敏感组和转染组HIF-1α、MDR1和Bcl-2 mRNA表达量明显低于耐药组（P<0.05)。Western blotting检测,敏感组和转染组HIF-1α、MDR1和Bcl-2蛋白表达量明显低于耐药组(P<0.05) ;免疫组织化学法,敏感组和转染组HIF-1α、MDR1和Bcl-2蛋白表达量明显低于耐药组(P<0.05);MDR1、Bcl-2 mRNA及蛋白在敏感组与转染组的表达量差异无统计学意义（P>0.05）。HIF-1α表达与MDR1、Bcl-2 mRNA表达量均呈正相关关系（r=0.908,P=0;r=0.916,P=0);HIF-1α表达与P-gp、Bcl-2蛋白表达呈正相关关系(r=0.773,P=0.003;r=0.862,P=0）。结论：HIF-1α沉默逆转人卵巢癌细胞顺铂耐药株SOV3/DDP耐药性可能与MDR1和Bcl-2表达降低有关联。
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MDR1 and MDR3 genes and drug resistance to cisplatin of ovarian cancer cells

Summary To investigate the relationship between MDR1 and MDR3 gene and drug resistance to cisplatin of ovarian cancer cells. Two siRNAs (MDR1, MDR3) which specifically targeted MDR1 and MDR3 genes were transfered into A2780/DDP cells. Then double staining with Annexin-V-FITC/PI was used to detect cell apoptosis by the flow cytometry (FCM). A2780/DDP cell viability was determined by MTT. MDR1 and MDR3 mRNA were assessed by RT-PCR. Caspase-3 protein was detected by Western blotting. Transfection of MDR1 and MDR3 siRNA into A2780/DDP cells failed to reverse the drug-resistance of A2780/DDP cells to cisplatin (P>0.05). No significant difference in the apoptosis efficiency was observed between the MDR1 and MDR3 siRNA, pSuppressorNeo vector transfection cells and untreated cells (P>0.05). In the presence of cisplatin of different concentrations, the viability of A2780/DDP cells was not significantly decreased after the transfection. No changes in MDR1 and MDR3 mRNA were found in MDR1 and MDR3 siRNA-transfected A2780/DDP cells. As compared with pSuppressorNeo and untreated groups, no significant difference existed in the expression of MDR1 and MDR3 mRNA (P>0.05). The expression of caspase-3 protein in MDR1 and MDR3 siRNA transfected A2780/DDP cells was not significantly increased. It is concluded that multidrug resistance induced by cisplatin in ovarian carcinoma cell lines is not due to overexpression of MDR1 and MDR3 gene. The drug resistance of ovarian carcinoma cells to cisplatin is not mediated by P-glycoprotein.     

miR-130a对卵巢癌A2780细胞顺铂耐药性的影响及其机制的研究

目的 探讨miR-130a表达的改变对卵巢癌A2780细胞（包括顺铂敏感细胞株A2780s和耐药株A2780/DDP）顺铂耐药性的影响及其机制。方法 将A2780s、A2780/DDP细胞各分为4组,分别予以单纯脂质体处理、转染阴性对照小RNA、miR-130a模拟物(可使miR-130a表达增加)、miR-130a抑制物(降低miR-130a表达)处理,MTS法检测各组细胞增殖情况和对顺铂的耐药性,RT-PCR、Western blot 法检测未处理和处理后细胞多耐药基因1（MDR1）、抑癌基因（PTEN） mRNA和蛋白的表达。结果 A2780/DDP细胞MDR1 mRNA和MDR1的表达产物P-糖蛋白(P-gp）的表达高于A2780s细胞（PMDR1 mRNA和P-gp表达水平;下调miR-130a的表达,同样不影响细胞的增殖, 但增强其对顺铂的敏感性, 并可降低MDR1 mRNA和P-gp的表达,提高PTEN蛋白的表达。结论 miR-130a抑制物通过上调PTEN蛋白和下调P-gp的表达来逆转卵巢癌A2780细胞系对顺铂的耐药性。miR-130a有望成为耐药性卵巢癌基因治疗的新靶点。     

白血病耐药细胞中葡萄糖神经酰胺合成酶对P-糖蛋白药物泵出功能的影响

目的探讨人白血病多药耐药细胞株K562/AO2中葡萄糖神经酰胺合酶（GCS）对P-糖蛋白（P-gp）泵出功能的影响,以便进一步研究GCS在白血病细胞耐药形成中的作用机制。方法采用RNA干扰技术分别靶向干扰K562/AO2中的GCS和多药耐药基因1（MDR1）,并通过荧光定量PCR检测小干扰RNA（siRNA）的干扰效果;用流式细胞术检测细胞内罗丹明123（rh123）的滞留量,以rh123的平均荧光强度（MFI）反映P-gp蛋白的泵出功能。结果 GCSsiRNA和MDR1siRNA对各自靶基因的抑制率分别是（68±5.72）%和（75.3±2.62）%;转染siRNA 48 h后,GCS干扰组MFI为255.75±76.1,MDR1干扰组MFI为357.25±41.57,分别是阴性干扰组的3.3倍和4.6倍。结论特异性的沉默GCS基因可以降低P-gp的泵出功能,提示GCS可通过协同P-gp的药物泵出功能参与白血病细胞的耐药形成过程。     

Reversal of MDR1 gene-dependent multidrug resistance using short hairpin RNA expression vectors

Background RNA interference using short hairpin RNA (shRNA) can mediate sequence-specific inhibition of gene expression in mammalian cells. A vector-based approach for synthesizing shRNA has been developed recently. Overexpression of P-glycoprotein (P-gp), the MDR1 gene product, confers multidrug resistance (MDR) to cancer cells. In this study, we reversed MDR using shRNA expression vectors in a multidrug-resistant human breast cancer cell line (MCF-7/AdrR). Methods The two shRNA expression vectors were constructed and introduced into MCF-7/AdrR cells. Expression of MDR1 mRNA was assessed by RT-PCR, and P-gp expression was determined by Western Blot and immunocytochemistry. Apoptosis and sensitization of the breast cancer cells to doxorubicin were quantified by flow cytometry and methyl thiazolyl tetrazolium (MTT) assays, respectively. Cellular daunorubicin accumulation was assayed by laser confocal scanning microscopy (LCSM). Statistical significance of differences in mean values was evaluated by Student’s t tests. P&lt;0.05 was considered statistically significant.Results In MCF-7/AdrA cells transfected with MDR1-A and MDR1-B shRNA expression vectors, RT-PCR showed that MDR1 mRNA expression was reduced by 40.9% (P&lt;0.05), 30.1% (P&lt;0.01) (transient transfection) and 37.6 % (P&lt;0.05), 28.0% (P&lt;0.01) (stable transfection), respectively. Western Blot and immunocytochemistry showed that P-gp expression was significantly and specifically inhibited. Resistance against doxorubicin was decreased from 162-fold to 109-fold (P&lt;0.05), 54-fold (P&lt;0.01) (transient transfection) and to 108-fold (P&lt;0.05), 50-fold (P&lt;0.01) (stable transfection). Furthermore, shRNA vectors significantly enhanced the cellular daunorubicin accumulation. The combination of shRNA vectors and doxorubicin significantly induced apoptosis in MCF-7/AdrR cells. Conclusions shRNA expression vectors effectively reduce MDR expression in a sustained fashion and can restore the sensitivity of drug-resistant cancer cells to conventional chemotherapeutic agents.     

Reversal of Adriamycin Resistance in Human Mammary Cancer Cells by Small Interfering RNA of MDR1 and MDR3 Genes

Resistance to antineoplastics is still the major cause of the failure of chemotherapy in cancer patients[1]. RNA interference (RNAi) is a conserved cellular mechanism in which double-stranded RNA silences the correspond-ing homologous cellular gene effectively and specificity. RNAi has a great potential of application in the reversal of drug resistance of tumor[2]. MDR1 and MDR3 are the two ATP binding cassette transporter genes. MDR3 is the second member of the human p-gp family next …     

TRAIL抑制胃癌多药耐药基因MDR1/P-gp的表达

目的观察肿瘤坏死因子相关凋亡诱导配体(TRAIL)对胃癌耐药细胞株SGC-7901/VCR多药耐药基因MDR1及其编码P-gp蛋白表达的影响,探讨以TRAIL为靶点逆转胃癌多药耐药的机制。方法 SGC-7901/VCR细胞株经不同浓度的TRAIL处理48 h后,RT-PCR检测各组胃癌细胞株中多药耐药MDR1 mRNA的表达情况,同时用ELISA法检测各组胃癌细胞株中P-gp表达的含量。结果不同浓度TRAIL(50、100、200、400μg/L)作用于细胞后,胃癌耐药细胞株SGC-7901/VCR的MDR1/P-gp表达受不同程度抑制,与对照组相比差异均具有统计学意义(P<0.05)。400μg/L与200μg/L组相比其MDR1/P-gp抑制程度并不明显,其余各组间差异均有统计学意义(P<0.05)。结论 TRAIL可抑制SGC-7901/VCR MDR1/P-gp的表达,且呈量效关系。TRAIL可能通过降低耐药基因MDR1的表达逆转胃癌的多药耐药。