寡聚体透明质酸逆转A549/DDP细胞耐药作用的研究

目的 研究寡聚体透明质酸逆转A549／DDP细胞耐药的作用。方法 MTT法研究寡聚体透明质酸对A549／DDP耐药逆转作用，流式细胞术测定细胞表面耐药相关蛋白P-gP、MRP的表达及凋亡调控蛋白P53、bcl-2的表达。结果 寡聚体透明质酸可提高A549／DDP对化疗药物的敏感性，使P-gp、MRP表达下降，P53表达增高。结论 寡聚体透明质酸有部分逆转A549／DDP耐药及诱导凋亡的作用。     

褪黑素逆转人乳腺癌细胞MCF-7／ADM对阿霉素耐药的作用机制

目的:探讨生理浓度(10-9 mol/L)和药理浓度(≥10-5 mol/L)褪黑素对耐阿霉素乳腺癌细胞系MCF-7/ADM 耐药的逆转作用及其机制.方法:应用四甲基偶氮唑蓝(MTT)法检测经不同浓度的褪黑素孵育后,阿霉素对MCF-7/ADM 细胞系半数抑制浓度IC50的改变.在电镜下观察单用阿霉素(20ug/ml)以及药理浓度的褪黑素(10-5mol/l)孵育后再应用阿霉素(20ug/ml)后MCF-7/ADM 细胞超微结构的变化.应用分光光度法测定MCF-7/ADM 和MCF-7/s细胞内GSH水平及褪黑素孵育后MCF-7/ADM和MCF-7/s细胞内GSH水平变化.结果:褪黑素孵育前阿霉素作用于MCF-7/ADM的IC50值为24.41ug/ml.经生理浓度(10-9mol/l)的褪黑素孵育后阿霉素IC50值为20.92ug/ml,两者经比较未见显著性差异(P=0.356).经浓度为10-5mol/L 和10-3mol/L的褪黑素孵育后阿霉素作用于MCF-7/ADMIC50值分别成为12.25ug/ml和10.46ug/ml,与孵育前阿霉素作用于MCF-7/ADM的IC50(24.41ug/ml)相比差异均具有显著性(P＜0.01).在电镜下均可观察到,经药理浓度(10-5mol/l)的褪黑素孵育后,阿霉素(20ug/ml)对细胞的损伤更为严重.经分光光度法测得MCF-7/ADM细胞内GSH水平明显高于MCF-7/s,生理浓度褪黑素并不能使MCF-7/ADM和MCF-7/s细胞内GSH水平明显降低(P=0.965),而药理浓度的褪黑素可以显著降低MCF-7/ADM和MCF-7/s细胞内GSH水平且具有一定的浓度依赖性(P＜0.01).结论:生理浓度的褪黑素对MCF-7/ADM的耐药未见明显影响,药理浓度的褪黑素对MCF-7/的ADM耐药性具有较明显逆转作用,其逆转机制可能与褪黑素对细胞内CSH水平调控有关.     

大黄素对乳腺癌多药耐药细胞株MCF-7/Adr的耐药逆转作用

目的：探讨中药成分大黄素(Emodin，EMD)对乳腺癌多药耐药细胞株MCF-7／Adr的耐药逆转作用。方法：药物敏感试验采用四唑氮盐(MTT)比色法，P糖蛋白以Western-blot法检测。结果：EMD在0～20μmol／L浓度时作用14天后对MCF-7／Adr未见明显毒性作用；EMD在10μmol／L浓度时，其耐药逆转倍数为1．7倍。EMD在20μmol／L浓度时，处理MCF-7／Adr2、4、6和11天后，检测P糖蛋白发现自第4天起P糖蛋白表达下降，至第11天无法检测到P糖蛋白的表达。结论：EMD具有逆转MCF-7／Adr多药耐药性的作用，可明显下调P糖蛋白的表达，且逆转作用持久。     

透明质酸寡糖调节A549/DDP多药耐药作用的研究

目的:通过研究透明质酸寡糖对人肺腺癌细胞系A549/DDP的P糖蛋白和多药耐药相关蛋白(MRP)、肺耐药蛋白(LRP)表达的影响,探讨透明质酸在引起肿瘤细胞多药耐药中的作用.方法: 将CD44单抗或透明质酸寡糖与A549/DDP细胞共培养48小时,放免法检测培养基中细胞所分泌透明质酸的含量,流式细胞仪检测经上述处理的A549/DDP表面MDR1 、MRP、LRP的表达率,MTT法检测在不同浓度顺铂作用下,各组细胞的存活率.结果: 经透明质酸寡糖处理后A549/DDP,分泌透明质酸较未处理组明显减少(P<0.05);且细胞表面与多药耐药相关的MDR1 、MRP、LRP的表达率均降低(P<0.05).另外,处理后的细胞,在不同浓度顺铂作用时,细胞凋亡率明显增加.结论: 体外条件下,透明质酸寡糖能逆转A549/DDP的耐药.     

PHⅡ-7对人乳腺癌多药耐药细胞MCF-7/ADR体外杀伤活性和逆转耐药作用

背景与目的:多药耐药(multidrug resistance,MDR)是恶性乳腺癌化疗失败的主要原因,而ABC转运蛋白家族的P-glycoprotein(P-gp)高表达是MDR的主要机制之一.因此研制能抑制P-gp表达及其功能的新型抗癌药是目前研究的热点.本研究旨在研究PH Ⅱ-7对人乳腺癌多药耐药细胞MCF-7/ADR体外抗瘤活性及逆转耐药的作用.方法:采用MTT法检测PHⅡ-7、多柔比星(adriamycin,ADR)及二者联合应用对人乳腺癌细胞MCF-7和耐药细胞株MCF-7/ADR的IC50值;采用流式细胞仪测定PH Ⅱ-7对MCF-7及MCF-7/ADR细胞凋亡的诱导作用;采用逆转录PCR和实时荧光定量PCR方法检测PHⅡ-7对多药耐药基因1(multidrug resistance gene 1,mdr1)表达水平的影响;通过流式细胞仪观察PHⅡ-7处理前后,MCF-7/ADR细胞内Rhodamine123浓度的改变,分析PHⅡ-7对p-gp外排功能的影响.结果:PH Ⅱ-7对MCF-7和MCF-7/ADR细胞均有生长抑制作用,IC50值分别为(6.07±0.85)和(5.51±1.22)μmol/L;低浓度PHⅡ-7与ADR联合应用能增强其细胞毒作用,二者具有协同作用.PHⅡ-7可诱导MCF-7和MCF-7/ADR细胞凋亡;在诱导凋亡过程中,PHⅡ-7可降低MCF-7/ADR细胞内mdrl基因的表达,抑制p-gp外排功能.结论:PHⅡ-7可诱导MCF-7/ADR凋亡,并具有对MCF-7相同的体外杀伤活性.PHⅡ-7可通过抑制P-gp的表达和功能逆转MCF-7/ADR耐药性.     

补骨脂素逆转K562/ADM多药耐药细胞系耐药性研究

目的:研究补骨脂素对白血病细胞阿霉素耐药株(K562/ADM)多药耐药(multidrug resistance,MDR)性的逆转作用及其机制.方法:采用MTT法检测药物细胞毒性作用,计算其逆转倍数.结果:补骨脂素在1～20μmol·L-1范围内,对K562和K562/ADM无明显细胞毒作用,但与ADM联合用药可使ADM对K562/ADM的IC50明显下降,补骨脂素(1～20μmol·L-1)能不同程度地降低ADM对K562/ADM细胞的IC50值.结论:补骨脂素能逆转K562/ADM细胞的多药耐药.     

三氧化二砷逆转人乳腺癌MCF-7/ADM细胞耐药的机制研究

目的　探讨三氧化二砷 (As2 O3 )对人乳腺癌MCF 7/ADM细胞耐药性的逆转作用及其相关机制。方法　采用MTT法检测As2 O3 的细胞毒性及非细胞毒性剂量 ,对MCF 7/ADM细胞药敏性的影响。以荧光分光光度计测定细胞内药物浓度的改变 ,明确As2 O3 对MCF 7/ADM的逆转作用。同时 ,于逆转前后分别采用生化方法测定谷胱甘肽S 转移酶 (GSTs)酶活性 ,RT PCR方法检测GST πmRNA表达水平的改变。结果　As2 O3 的非细胞毒性剂量为 0 .2 μmol/L ,低毒剂量为 0 .8μmol/L。0 .2 μmol/LAs2 O3 可增加MCF 7/ADM细胞内阿霉素 (ADM)浓度 ,使细胞MCF 7/ADM的IC50 由原来的5 3.74 μmol/L降低至 2 5 .0 μmol/L ,其逆转倍数为 2 .1倍。在 0 .2 μmol/L、0 .8μmol/LAs2 O3 作用前后 ,GSTs酶活性有显著性改变 ,由 2 9.6 8± 0 .2 9(U/ml)分别降低为 19.2 9± 2 .10 (U/ml)、12 .6 6± 2 .78(U/ml) ,P <0 .0 5 ,而GST πmRNA的表达水平也呈不同程度的下调。结论　As2 O3 可部分逆转人乳腺癌MCF 7/ADM细胞对ADM的耐药性 ,其逆转机制可能与细胞内GST π的改变有关。     

人类白血病多药耐药细胞株K562/ADM、HL60/ADM的耐药性及耐药逆转的研究

目的：研究K562／ADM、HL60／ADM的耐药性及CsA对其耐药的逆转作用。方法：MTT比色法检测细胞耐药性及CsA对细胞耐药性的影响，流式细胞仪检测Pgp、MRP的表达及细胞内柔红霉素(DNR)的浓度。结果：K562／ADM、HL60／ADM对DNR、ADM、VCR、Har、VP16、MIT交叉耐药，对Acla和Ara—C基本不耐药。K562／ADM细胞Pgp过度表达，HL60／ADM细胞的MRP过度表达。CsA使K562／ADM、HL60／ADM细胞内药物浓度增加，逆转了K562／ADM、HL60／ADM的耐药性，而对K562、HL60的耐药性基本无影响。结论：两种不同耐药机制的细胞株对8种常用化疗药物的耐药谱相似，对Acla基本不产生耐药性，故在防止和克服多药耐药的基础上，Acla可能取代DNR、ADM。环孢菌素A(CsA)对两种不同耐药机制的细胞株的耐药性均有逆转作用，主要是通过增加胞内药物浓度来达到逆转作用。     

二甲亚砜对K562/ADM耐药细胞株耐药性的逆转作用

目的：研究二甲亚砜对K562／ADM耐药细胞的逆转作用。方法：通过加入二甲亚砜后耐药细胞的生长情况，逆转倍数的计算，细胞内过氧化物染色的阳性程度以及电镜下观察耐药细胞诱导前后的变化。结果：二甲亚砜诱导K562／ADM耐药细胞前后生长情况有显著差异且逆转借故为4．0，Pox染色阳性程度明显递增，电镜下可观察诱导后K562／ADM耐药细胞有向成熟分化趋势。结论：二甲亚砜对逆转K562／ADM的耐药性是有益的。     

甲基莲心碱对耐阿霉素人乳腺癌细胞多药耐药性的逆转

目的研究甲基莲心碱逆转耐阿霉素人乳腺癌细胞多药耐药性(MDR)的作用及机制。方法采用噻唑蓝(MTT)比色法检测细胞毒性;PI 染色流式细胞计数测定细胞凋亡;间接免疫荧光流式细胞术检测细胞 P-gp 的表达;HPLC 检测细胞内药物浓度。结果 Nef(1、5、10μmol·L~(-1))对人乳腺癌细胞(MCF-7/S)和耐阿霉素人乳腺癌细胞(MCF-7/ADM)无显著毒性作用。阿霉素(ADM)对敏感株 MCF-7/S 的 IC_(50)为0.13μg·mL~(-1)而对 MDR 细胞株 MCF-7/ADM 的 IC_(50)为11.63μg·mL~(-1),MCF-7/ADM 细胞较MCF-7/S 细胞对 ADM 耐药88倍,1、5、10μmol·L~(-1) Nef 能使 ADM 对 MCF-7/ADM 细胞的 IC_(50)从11.63μg·mL~(-1)依次下降至4.59、2.44、0.27μg·mL~(-1)。MCF-7/ADM 细胞对 ADM 具有凋亡抗性,Nef(1、5、10μmol·L~(-1))能克服 MCF-7/ADM 细胞对 ADM 的凋亡抗性。MCF-7/ADM 细胞较 MCF-7/S 细胞高表达 P-gp,Nef(10μmol·L~(-1))处理24h 后,MCF-7/ADM 细胞 P-gp 表达明显下降。ADM 作用3h 后,MCF-7/ADM 细胞内 ADM 的浓度比 MCF-7/S 细胞少2.8倍,Nef(10μmol·L~(-1))可使 MCF-7/ADM 细胞内 ADM 的浓度增加3.2倍,但并不增加 MCF-7/S 细胞内 ADM 的浓度。结论 Nef 具有逆转耐阿霉素人乳腺癌细胞 MDR 的作用,其作用机理与促进 MDR 细胞内 ADM 积累和下调 MDR 细胞 P-pg 表达有关。     

甲基莲心碱对耐阿霉素人乳腺癌细胞多药耐药性的逆转

Objective: To study the reversal effect of neferine on adriamycin (ADM) resistant human breast cancer cell line MCF-7/ADM. Methods: The cytotoxic effect of Nef or ADM was determined by 3-[4, 5-dimethylthiazol-2.-yl], 5-diphenyl tetraxolium bromid (MTT) assay. Apoptosis and the expression of P-glycoprotein (P-gp) were detected by flow cytometry (FCM). The intracellular ADM concentration was measured by HPLC. Results: Nef at 1, 5, 10 mol/L decreased the IC₅₀ of ADM to MCF-7/ADM from 11.63 g/mL to 4.59, 2.44, 0.27 g/mL respectively. MCF-7/ADM could resist the apoptosis induced by ADM while Nef (1-10 mol/L) could augment ADR-mediated apoptosis. Nef (10 mol/L) increased the accumulation of ADM up to 2.88 fold in MCF-7/ADM but not in sensitive cells MCF-7/S and reduced the expression of P-gp in MCF-7/ADM cells. Conclusion: Nef can circumvent multidrug resistance (MDR) of MCF-7/ADM cells and the mechanism was associated with the increase of intracellular accumulation of ADM and the reduced expression of P-gp in MCF-7/ADM cells.     

去磷酸化RB蛋白表达对阿霉素诱导MCF-7/S细胞凋亡的影响

目的检测经阿霉素(ADR)处理的人乳腺癌MCF-7/S细胞的凋亡率(AR)及去磷酸化RB蛋白表达的变化,以探讨ADR诱导细胞凋亡的可能机理。方法将体外培养的MCF-7/S细胞分为实验组(以不同浓度ADR处理细胞)及对照组(以等体积的生理盐水处理细胞);应用MTT比色法检测ADR对MCF-7/S细胞的抑制率(IR);应用流式细胞术检测实验组和对照组细胞的AR;采用S-P免疫组化染色法检测ADR作用后去磷酸化RB蛋白表达的变化。结果ADR抑制MCF-7/S细胞增殖,呈剂量依赖性,IC50为0.128mg/L;0.25、2、5μg/mlADR处理的MCF-7/S细胞的AR分别为0.171、0.184、0.259,而对照组MCF-7/S细胞的AR为0.045,两者比较,有非常显著性差异(P<0.01);5μg/mlADR实验组MCF-7/S细胞的去磷酸化RB蛋白的表达量为986.8±207.4,而对照组为131.7±31.9,两者比较,有非常显著性差异(P<0.01);5μg/mlADR实验组MCF-7/S细胞的AR与其去磷酸化RB蛋白的表达量呈正相关(γ=0.998,P=0.037)。结论ADR能抑制MCF-7/S细胞增殖并诱导其凋亡,其机理可能与去磷酸化RB蛋白表达水平上调有关。     

脉冲磁场逆转乳腺癌细胞多药耐药性的作用研究

目的: 研究脉冲磁场(Pulsed Magnetic Fields,PMF)对乳腺癌耐药细胞株MCF-7/ADR的逆转作用. 方法: 采用MTT实验方法,分别检测不同频率及不同磁场强度条件照射下的MCF-7/ADR细胞的耐药倍数和逆转倍数.用流式细胞术检测经脉冲磁场照射后MCF-7/ADR细胞中Rh123药物蓄积量变化.用流式免疫荧光技术检测膜经脉冲磁场照射后MCF-7/ADR细胞膜表面P-糖蛋白(p-gP)和多药耐药相关蛋白(MRPI)表达情况.采用半定量RT-PCR(逆转录-聚合酶链反应)检测经脉冲磁场照射后MCF-7/ADR细胞中MDR1和MRP1基因表达情况.建立人乳腺癌耐药细胞株MCF-7/ADR裸鼠移植瘤模型,通过测量肿瘤体积及重量观察PMF时肿瘤细胞的体内逆转作用. 结果: 脉冲磁场能有效逆转乳腺癌耐药细胞株MCF-7/ADR对阿霉素产生的耐药性(P<0.01),其中110Hz,40mT照射条件逆转效果最好,可达5倍左右;脉冲磁场能提高罗丹明123在细胞内的蓄积量.其中110Hz,40mT照射条件下可有效提升20%左右药物蓄积量;细胞经脉冲磁场照射后,膜表面耐药蛋白P糖蛋白表达量明显下降,MRP1蛋白表达量变化不明显;编码上述两种耐药蛋白的耐药基因表达量均明显下降;此外,脉冲磁场联合阿霉素可有效逆转裸鼠移植瘤的生长增值(P<0.01). 结论: PMF具有逆转体外和体内乳腺癌细胞多药耐药性的作用.     

Effects of Rapamycin on Cell Apoptosis in MCF-7 Human Breast Cancer Cells

Background: Rapamycin is an effective anti-angiogenic drug. However, the mode of its action remainsunclear. Therefore, in this study, we aimed to elucidate the antitumor mechanism of rapamycin, hypotheticallyvia apoptotic promotion, using MCF-7 breast cancer cells. Materials and Methods: MCF-7 cells were platedat a density of 15105 cells/well in 6-well plates. After 24h, cells were treated with a series of concentrations ofrapamycin while only adding DMEM medium with PEG for the control regiment and grown at 37oC, 5% CO2and 95% air for 72h. Trypan blue was used to determine the cell viability and proliferation. Untreated andrapamycin-treated MCF-7 cells were also examined for morphological changes with an inverted-phase contrastmicroscope. Alteration in cell morphology was ascertained, along with a stage in the cell cycle and proliferation.In addition, cytotoxicity testing was performed using normal mouse breast mammary pads. Results: Our resultsclearly showed that rapamycin exhibited inhibitory activity on MCF-7 cell lines. The IC50 value of rapamycin onthe MCF-7 cells was determined as 0.4μg/ml (p<0.05). Direct observation by inverted microscopy demonstratedthat the MCF-7 cells treated with rapamycin showed characteristic features of apoptosis including cell shrinkage,vascularization and autophagy. Cells underwent early apoptosis up to 24% after 72h. Analysis of the cell cycleshowed an increase in the G0G1 phase cell population and a corresponding decrease in the S and G2M phasepopulations, from 81.5% to 91.3% and 17.3% to 7.9%, respectively. Conclusions: This study demonstrated thatrapamycin may potentially act as an anti-cancer agent via the inhibition of growth with some morphologicalchanges of the MCF-7 cancer cells, arrest cell cycle progression at G0/G1 phase and induction of apoptosis inlate stage of apoptosis. Further studies are needed to further characterize the mode of action of rapamycin asan anti-cancer agent.     

Cytotoxicity Enhancement of Paclitaxel by Loading on Stearate-g-dextran Micelles on Breast Cancer Cell Line MCF-7

Objective: Paclitaxel (PTX) is a chemotherapeutic agent used for treating breast cancer. The study aimed to preparePTX loaded dextran stearate (Dex-SA) and evaluate its efficacy against human breast cancer cell line MCF-7. Methods:Dex-SA/PTX micelles were prepared by dialysis method. The micelles size, zeta potential and particle size distributionwere measured by dynamic laser light scattering method. Amount of loaded PTX on the polymer measured by HPLC.Release profiles of the drug from the micelles were obtained in buffer (phosphate pH=7.4). Then the cytotoxicity of blankmicelles, Dex-SA/PTX micelles and free PTX were evaluated in the MCF-7 cells by MTT method. Result: Loadingefficiency of PTX on the Dex-SA was measured about 84.24±9.07%. The smallest particles size was about 193.9±7.1nm but the other formulation with larger particle size had better zeta potential (-33.5±6.74 mV). The drug releasefrom the micelles was slowly and reached steady state after about 12 hours. The cytotoxicity experiment showed thatDex-SA/PTX micelles have more cytotoxicity compared to free PTX against MCF7 cell lines. Conclusions: Dex-SApolymeric micelle is a suitable carrier for hydrophobic cytotoxic drugs such as PTX.     

人参皂甙Rg3诱导乳腺癌细胞系 MCF-7凋亡的实验研究

背景与目的:人参皂甙Rg3[20(R)-GinsenosideRg3]是从红参中提取的微量中药单体。近年研究表明人参皂甙Rg3尚具有抑制肿瘤细胞的增殖、抗肿瘤细胞浸润和转移等作用。肿瘤的发生和发展是一个极其复杂的过程,有多种转移相关的蛋白因子参与,并涉及多种转移途径和分子机制。人参皂甙Rg3抗肿瘤机制的研究为目前中药抗肿瘤研究热点之一。本研究的目的在于探讨Rg3抑制乳腺癌细胞的作用及其诱导凋亡的机制。材料与方法:四甲基偶氮唑蓝(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide,MTT)法检测人乳腺癌细胞MCF-7的细胞增殖活力;荧光染色观察凋亡细胞的形态学变化;流式细胞术分析细胞周期及细胞凋亡;琼脂糖凝胶电泳测定DNA梯状带。结果:Rg3与MCF-7细胞生长抑制率之间有浓度依赖关系,相关系数(r)=0.953,Rg3处理细胞48h的IC50为71.91μg/ml;荧光显微镜下观察到经Rg3作用后,MCF-7细胞出现染色质凝集、核片段化、凋亡小体等凋亡形态学特征;流式细胞术检测表明Rg3能诱导细胞凋亡及调节细胞周期,用150μg/ml的Rg3处理细胞48h后,S期和G2-M期的细胞比率增加,G0-G1的细胞比率下降。细胞凋亡率从对照组的(0.45±0.25)%上升到(34.86±4.65)%。DNA琼脂糖凝胶电泳结果显示,服150μg/ml的Rg3处理细胞24h和48h后,能够使细胞产生明显的梯形电泳图谱(DNAladder)。结论:Rg3可通过诱导MCF-7细胞凋亡而发挥其抑制细胞增殖的作用。     

Oxidants-Antioxidants Profile in the Breast Cancer Cell Line MCF-7

Reactive oxygen species (ROS) have various biological effects and they are non-linear in characteristic. In high oxidativestress, they may cause cytotoxicity, inhibit cell proliferation, and induce cell death in the form of apoptosis/necrosis;while in low or medium oxidative stress, ROS may cause DNA damage, cell mutation, inflammation, cell proliferation,and eventually they may induce carcinogenesis. Antioxidants are compounds with the ability to reduce ROS. Cell lineMCF-7 is one of the breast cancer cell lines that is known to have small amount of antioxidant MnSOD compared to theother cell lines. Low antioxidant MnSOD level in breast cancer cell line MCF-7 leads to low concentration of hydrogenperoxide, because antioxidant MnSOD will convert radical superoxide to hydrogen peroxide. The aim of this researchwas to analyze oxidants and antioxidants profile in breast cancer cell line MCF-7 and their relationship with cell number.Observations were conducted for 5 days. The cell number was counted with tryphan blue method and haematometer.The concentration of radical superoxide was measured with DHE staining using LSCM tipe Olympus Fluoview FV1000-Ver 1.7. MnSOD activity, hydrogen peroxide concentration, and catalase activity were measured with ELISA.The results showed that the longer of observation, the greater concentration of oxidants and MnSOD activity, but therewas no change in catalase activity. Conclusion the increase in cancer cells number is influenced by radical superoxide.     

FasL基因转染对人乳腺癌MCF-7细胞药物敏感性的上调效应

目的:探讨FasL基因转染对肿瘤细胞化疗敏感性的调节效应,方法:LjpofectAMINE介导建立FasL基因修饰的乳腺癌细胞系MCF-7(?)FL,MTT法检测化疗药物对转染细胞的杀伤效应,半定量RT-PCR分析化疗药物作用前后转染细胞Fas mRNA表达水平变化,结果:经C418筛选,RT-PCR和免疫组化鉴定,建立FasL稳定表达MCF-7/FL,ADM在0.625～2.5μg′ml之间.MTX在3～6μg′ml.CDDP在1.25～10μg ml间对MCF-7FL的杀伤效应均明显高于MCF-7和转染空载体的MCF-7Vt而F(ab’)_2-APO-LMcAb可部分抑制这—增强效应,半定量RT-PCR显示上述化疗药物作用后MCF-7/FL Fas mRN水平表达显著增强,结论:外源FasL基因导入可上调肿瘤细胞对多种化疗药物的敏感性,其机制可能与化疗药物上调Fas表达从而增强瘤细胞FasL-Fas凋亡通路效应有关