Empirical studies about quercetin increasing chemosensitivity on human lung adenocarcinoma cell line A549

Objective： The present study was designed to investigate whether quercetin exerts increasing chemosensitivity on human lung adenocarcinoma cells when quercetin combined with cisplatin （DDP） and vincristine （VCR） in vitro respectively and its possible antitumor mechanism. To provide experimental proof for clinical combination application. Methods： Using intermittent administration of high dose VCR, human lung adenocarcinoma sensitive cell line （A549/S） was induced to VCR- resistant human lung adenocarcinoma cell line （A549NCR）. MTT assay was adapted for examing the 50% inhibition （IC50） value of DDP and VCR on A549/S and A549/VCR when quercetin combined with DDP and VCR respectively. Results： IC50 of DDP on A549/S and A549/VCR was 10.18 and 12.35 mg/L, and the IC50 of VCR on the two cell lines was 1.21 and 12.77 rag/L, respectively. The resistance fold of A549/VCR on VCR and DDP was 10.55 and 121, respectively. When quercetin at concentration of 50, 100 and 200 pmol/L in combination with DDP and VCR respectively, the IC50 of DDP and VCR on A549/S and A549/VCR were obvious decreased （P 〈 0.05 - P 〈 0.01）. Conclusion： The experiment results suggested that quercetin could increase the chemosensitivity and partly revise the resistance of A549NCR.

Effects of paclitaxel on cell proliferation and apoptosis and its mechanism in human lung adenocarcinoma A549 cells

Objective： To investigate the effect of paclitaxel on cell proliferation and apoptosis of human lung adenocarcinoma A549 cells line and its mechanism in vitro. Methods ： Cell growth inhibition of paclitaxel on A549 cells was analyzed by MTT assay. Cell apoptosis was detected by DNA cytofluorometry, Hoechst33258 staining when treated with paclitaxel for 48 hours. Meanwhile, Cell cycle and apoptotic rate were analyzed by flow cytometry. The protein expressions of Bax and Bcl-2 were studied by Western Blot. Results： Paclitaxel inhibited the proliferation of A549 cells in a time-and dose-dependant manner. Hoechst33258 staining indicated that apoptosis was induced by paclitaxel. After treated for 48 hours, cell apoptosis rates of 25 nmo1/L, 50 nmol/L and 100 nmol/L paclitaxel groups were 11.52 ± 1.94% ,17.73 ±2.53%, and 29.32 ±5.51% respectively, which were significantly higher than those of control group 5.88 ±1.07%（all P 〈 0.01 ）, and apoptosis rate increased in dose-dependant manner. Meanwhile, G2/M stage cell percentage of 25 nmol/L, 50 nmol/L and 100 nmol/L paclitaxel groups were 42.52 ± 6.25%, 40.46 ± 5.81%, and 35.34 ±6.17% respectively,which were significantly higher than that of control group 22.32 ± 3.30%（all P 〈 0.01 ）; Western blot showed that paclitaxel increased the expression of Bax and decreased the expression of Bcl-2 in dose-dependant manner. Conclusion： Paclitaxel can inhibit A549 cell proliferation in a time-and dose-dependant manner. Its mechanism may be related to arresting cell cycle in G2/M stage and induce cell apoptosis by up-modulating Bax expression and down-modulating Bcl-2 expression.

Reversal effect of recombinant human Endostatin on cisplatin resistance in A549/DDP human lung adenocarcinoma cells in vitro

Objective： Recombinant human Endostatin （rh-Endostatin, YH-16） can reverse cisplatin resistance in A549/DDP cells. However, the possible effect of rh-Endostatin in reversing DDP-resistance in A549/DDP cells and the mechanism are needed to be investigated. Methods： Lung adenocarcinoma cell line A549 and its DDP-resistant cell line A549/DDP were treated with DDP and/or recombinant human Endostatin. Difference in drug resistance was analyzed between different regi- mens and between different cell lines after a 72 h-treatment in vitro. And below the non-cytotoxic concentration of rh-End- ostatin, the possibility of rh-Endostatin in reversing DDP-resistance in A549/DDP was evaluated. The resistance protein which was detected in the study included P glycoprotein （P-gp） and topoisomerase II （Topo-II）. Results： Rh-Endostatin below 400 IJg/mL showed no cytotoxicity in either A549 or A549/DDP after 72 h-treatment with it. The inhibited concentration of 50% （IC50） observed for DDP was （0.79 _＋ 0.05） IJg/mL in A549 and （13.2 ＋ 1.1） in A549/DDP respectively. IC50 was reduced to 2.57 ＋ 0.05 #g/mL in A549/DDP treated by rh-Endostatin below the non-cytotoxic concentrations in combination with DDP, with a reversal fold （RF） of 5.14 and a relative reversal rate of 85.6%. Apoptotic rates were 2.01%, 13.47% and 29.26% re- spectively for cells treated with rh-Endostain, DDP, and the combination. The rate of the A549/DDP control group was 0.99%. The expression level of P-gp or Topo-II was higher in A549/DDP cells than in A549 cells. Rh-Endostatin may partially reverse DDP-resistance in A549/DDP cells in vitro, with a probable mechanism related to lowering expression of P-gp and Topo-II. Conclusien： Rh-Endostatin of non-cytotoxic dose partially reversed cisptatin resistance in cisplatin-resistant human lung adenocarcinoma cell line A549/DDP. Rh-Endostatin reversed the resistance of A549/DDP cells to DDP, which may be related to decreased protein expression of P-gp and Topo-II in A549/DDP cells.

Inhibitory effect of toremifene monotherapy or combined with gemcitabine on A549 human lung adenocarcinoma cells

Objective： The aim of this study was to investigate the effect of toremifene on A549 human lung adenocarci- noma cells, and its sensibilization with gemcitabine, so that to provide a new clinical approach for non-small-cell lung cancer （NSCLC）. Methods： A549 cells were seeded into 96-well plates and exposed to different agents （gemcitabine or gemcitabine with toremifene）. The cytotoxicity of each agent was evaluated by MTT, cell cycle and apoptotic rate were detected by flow cytometry （FCM）. Results： 1. By using FCM, we found A549 cells in S and G2/M phases with toremifene decreased but increased in G0/G1 phase. The higher concentration of toremifene, the more decreased was when compared with the control group. 2. FCM showed toremifene＇s apoptosis effect on A549 cells increased with its increasing dose. 3. By MTT, toremifene had no cytotoxic effect on A549 cells at the concentration of 5 or 2.5 pmol/L. The IC5o of gemcitabine to A549 was 34.51 tJmol/L, and the combined group was 13.59 pmol/L. Conclusion： Toremifene could inhibit the growth of A549 human lung adenocarcinoma cells. Toremifene combined with gemcitabine showed significantly remarkable chemotherapy sensibilization on A549 human lung adenocarcinoma cells.

Study of Pravastatin on Intervention of the Apoptosis in Human Lung Adenocarcinoma A549

Lung cancer is one of the serious threats to human health and life of malignant diseases, on a global scale; it has become one of the major lung cancer deaths. Due to the growth of the tumor and the main reason is that apoptosis is inhibited, therefore, it can induce apoptosis in lung cancer cells that is an important measure for the treatment of lung cancer, which is one of the effective means to reduce lung cancer mortality. In this paper, A549 human lung adenocarcinoma cell line, for example, has the use of chemical genetics of these emerging technological platforms, research pravastatin on apoptosis in human lung adenocarcinoma A549 intervention, while providing a theoretical basis for the development of new lung cancer therapy.

The Inhibitory Effects of Rh-endostatin(YH-16) in Combination with Radiotherapy on Lung Adenocarcinoma A549 in Mice and the Underlying Mechanisms

In order to investigate the inhibitory effects of Endostar(rh-endostatin,YH-16)in combination with radiotherapy on lung adenocarcinoma A549 in mice and the interaction mechanisms of combined therapy,the transplantation tumor models of A549 lung adenocarcinoma were established.When the largest diameter of tumor reached 1.0cm,all nude mice were randomly divided into 4 groups:Endostar group,radiotherapy group,radiotherapy plus Endostar(combined treatment)group,and control group(n=6 in each group).The largest d...

Highly Efficient Labeling of Human Lung Cancer Cells Using Cationic Poly-L-lysine-Assisted Magnetic Iron Oxide Nanoparticles

Cell labeling with magnetic iron oxide nanoparticles(IONPs)is increasingly a routine approach in the cellbased cancer treatment.However,cell labeling with magnetic IONPs and their leading effects on the biological properties of human lung carcinoma cells remain scarcely reported.Therefore,in the present study the magnetic c-Fe2O3nanoparticles(MNPs)were firstly synthesized and surface-modified with cationic poly-L-lysine(PLL)to construct the PLL-MNPs,which were then used to magnetically label human A549 lung cancer cells.Cell viability and proliferation were evaluated with propidium iodide/fluorescein diacetate double staining and standard 3-(4,5-dimethylthiazol-2-diphenyl-tetrazolium)bromide assay,and the cytoskeleton was immunocytochemically stained.The cell cycle of the PLL-MNPlabeled A549 lung cancer cells was analyzed using flow cytometry.Apoptotic cells were fluorescently analyzed with nuclear-specific staining after the PLL-MNP labeling.The results showed that the constructed PLL-MNPs efficiently magnetically labeled A549 lung cancer cells and that,at low concentrations,labeling did not affect cellular viability,proliferation capability,cell cycle,and apoptosis.Furthermore,the cytoskeleton in the treated cells was detected intact in comparison with the untreated counterparts.However,the results also showed that at high concentration(400 lg m L-1),the PLL-MNPs would slightly impair cell viability,proliferation,cell cycle,and apoptosis and disrupt the cytoskeleton in the treated A549 lung cancer cells.Therefore,the present results indicated that the PLL-MNPs at adequate concentrations can be efficiently used for labeling A549 lung cancer cells and could be considered as a feasible approach for magnetic targeted anti-cancer drug/gene delivery,targeted diagnosis,and therapy in lung cancer treatment.

芝麻素对长春瑞滨诱导人肺腺癌A549细胞凋亡的影响

[目的]探讨芝麻素对长春瑞滨诱导人肺腺癌A549细胞株凋亡的影响.[方法]选择人肺腺癌A549细胞株进行体外传代培养,制备成浓度为1.0×105个/mL的细胞悬浮液并接种于96孔板中.实验设空白组(加入DMEM培养液)、对照组(加入DMEM培养液及人肺腺癌A549细胞株)、芝麻素组(芝麻素10、20、30、40、50、60、70、80、90、100μg/mL)、长春瑞滨组(长春瑞滨5、10、15、20、25、30、35μg/mL)及联合用药组(加入IC50浓度的芝麻素和长春瑞滨,IC50为后续联合用药组实验药物浓度).空白组加入160μL的DMEM培养液,对照组及实验组各加入160μL已制备好的人肺腺癌A549细胞株悬浮液,待细胞株贴壁后,空白组、对照组及实验组分别加入20μL的生理盐水和20μL各相关浓度的药物.采用MTT法检测细胞增殖能力,利用倒置显微镜及HE染色法观察细胞形态学变化,采用流式细胞仪检测细胞凋亡情况.[结果]在10~100μg/mL质量浓度范围内,低质量浓度的芝麻素具有抑制A549细胞株增殖的作用,IC50质量浓度为40μg/mL;在5~35μg/mL质量浓度范围内,长春瑞滨具有抑制A549细胞株增殖的作用,且随着药物质量浓度升高细胞抑制率升高,IC50质量浓度为20μg/mL;芝麻素与长春瑞滨联合用药对A549细胞株的抑制率明显高于单药用药(P<0.01).倒置显微镜及HE染色法观察结果显示,与对照组比较,芝麻素(40μg/mL)、长春瑞滨(20μg/mL)及联合用药(芝麻素40μg/mL+长春瑞滨20μg/mL)作用于A549细胞株48 h后贴壁细胞数量均明显减少,细胞间连接疏松,贴壁能力减弱,部分细胞体积变小、变圆或呈不规则形,核染色质凝集,细胞膜起泡形成凋亡小体,失去原有肿瘤细胞多角形或梭形形态,且联合用药组较单药组上述变化更为明显.流式细胞仪检测结果显示,药物作用48 h后,芝麻素组(40μg/mL)、长春瑞滨组(20μg/mL)及联合用药组(芝麻素40μg/mL+长春瑞滨20μg/mL)细胞凋亡率均明显高于对照组(P<0.01),且联合用药组早期凋亡率明显高于单独用药组(P<0.01).[结论]芝麻素可增强长春瑞滨诱导人肺腺癌A549细胞凋亡的作用.

Clinical Observation on Treatment of NonParvicellular Carcinoma of the Lung with Jin Fu Kang Oral Liquid

Jin Fu Kang Oral Liquid ([symbol: see text]), made of traditional Chinese drugs for supplementing qi and nourishing yin, was developed according to the common symptoms in lung carcinoma with deficiency of both qi and yin. Of the 96 cases in the Jin Fu Kang group, 1 case got complete remission (CR) after treatment, 8 cases partial remission (PR), 52 cases no change (NC), PR + NC covering 63.5%. Of the 52 cases in the group of Jin Fu Kang plus chemotherapy, 11 cases got PR after treatment, 26 cases NC, PR + NC covering 71.2%. Of the 25 cases in the chemotherapy group, 4 cases got PR after treatment, 11 cases NC, PR + NC covering 60.0%. The results show that the therapeutic effectiveness in the Jin Fu Kang group and the group of Jin Fu Kang plus chemotherapy was better than that in the chemotherapy group. The one-year survival rate and the two-year survival rate after treatment in the Jin Fu Kang group were 67.3% and 67.3% respectively; 66.7% and 66.7% in the group of Jin Fu Kang plus chemotherapy; and 40.3% and 0.0% in the chemotherapy group. The improvement of clinical symptoms, increase of body weight and improvement of health situation (KPS marks) after treatment in both the Jin Fu Kang group and the group of Jin Fu Kang plus chemotherapy were better than that in the chemotherapy group. Some indicators of immunology and hemogram after treatment were greatly improved in the Jin Fu Kang group, worse in the chemotherapy group, but no obvious improvement in the group of Jin Fu Kang plus chemotherapy.

Inhibitory Effect of Cantharidin on Proliferation of A549 Cells

Objective： To study the inhibition of Cantharidin against the proliferation of human lung cancer A549 cells and its mechanism. Methods： MTT assay was employed to determine the inhibition of Cantharidin against proliferation of A549 cells and flow Cytometry was applied to analyze A549 cell cycle and the effect of Cantharidin on cell cycle. Results： Cantharidin showed inhibition against the proliferation of A549 cells, and the inhibition was mediated by blocking A549 cell cycle at G2/M phase significantly. Conclusion： Cantharidin exhibits inhibition against the proliferation of human lung cancer A549 cells.

miR-33a-5p靶基因分析验证及对人肺腺癌A549细胞增殖的影响

目的研究miR-33a-5p过表达对人肺腺癌A549细胞增殖的影响及探索其可能的机制。方法在A549细胞中瞬时转染miR-33a-5p mimics,CCK-8和BrdU实验检测细胞增殖能力,转录组测序(RNA-seq)检测mRNA表达水平,targetscan(8.0)、miRDB(2020)、miRWalk(release_2022_01)和ENCORI(starbase,v2.0)联合筛选miR-33a-5p的潜在靶基因,并与RNA-seq的下调表达的基因取交集,RT-qPCR进行基因表达验证。结果RT-qPCR结果显示,miR-33a-5p在A549细胞中高表达(P<0.05);CCK-8实验和BrdU实验结果显示,细胞增殖能力受到抑制(P均<0.05);RNA-seq结果显示,差异基因共494个,其中上调266个,下调228个;GO功能富集主要在细胞外区组成、质膜的组成、受体复合物、细胞外泌体、细胞外基质结构组成、钙离子结合等,KEGG富集主要在补体和凝血途径、胰岛素抵抗、ABC转运途径、IL-17途径、NOD样受体途径和NF-κB信号通路等;靶基因预测分析和RT-qPCR表达验证显示,MTHFD2、OSBPL6、HADHB、HMGCLL1、GUCY1A2和DEPTOR是miR-33a-5p的潜在靶基因(P均<0.05)。结论miR-33a-5p可能通过调控MTHFD2、OSBPL6、HADHB、HMGCLL1、GUCY1A2和DEPTOR基因转录后表达水平来抑制A549细胞的增殖。

牡蛎低分子活性肽BPO-L对人肺腺癌A549细胞周期和相关癌基因、抑癌基因表达的调控作用

采用酸抽提、凝胶柱层析等方法,从僧帽牡蛎体内分离提取到牡蛎低分子活性多肽组分BPO-L,以HMBA处理组为平行对照,流式细胞仪检测细胞周期变化及以免疫细胞化学方法检测相关癌基因、抑癌基因表达变化.研究BPO-L对人肺腺癌A549细胞分化的生物学效应,探索其对肺癌细胞的作用机理.实验结果显示,BPO-L能有效抑制A549细胞增殖活动,促使细胞阻滞于G0/G1期.在此过程中,A549细胞c-myc,MTp53等癌基因蛋白表达减弱,p21WAF1/CIP1和Rb等抑癌基因蛋白表达活性的增强.本研究证实BPO-L对肺癌细胞具有显著的诱导分化作用.其诱导癌细胞分化机理与其调节和干预c-myc、MTp53等癌基因与p21WAF1/CIP1和Rb等抑癌基因的表达有关.

丹参酮ⅡA诱导人肺腺癌A549细胞凋亡

目的探讨丹参酮ⅡA(TanshinoneⅡA,TanⅡA)抗人肺腺癌A549作用及其可能作用机制。方法通过细胞形态学和MTT法观察TanⅡA对A549细胞增殖的影响;应用Hoechest33258和PI双染法观察细胞凋亡;采用荧光分光光度计检测细胞内钙及线粒体膜电位;RT-PCR检测Bad和MT-1A mRNA的表达。结果 TanⅡA能抑制A549细胞增殖,且随TanⅡA剂量的增加和作用时间的延长而增强,TanⅡA作用A549细胞24、48和72h的IC50分别为117.85、14.87和6.89μmol·L-1。TanⅡA作用A549细胞24h后,A549细胞出现染色质聚集等典型的凋亡形态学改变,且随TanⅡA剂量的增加,A549细胞凋亡百分率逐渐增大。TanⅡA作用后,A549细胞的细胞内钙升高、线粒体膜电位降低、Bad mRNA表达增加、MT-1A mRNA表达下调。结论 TanⅡA具有抗A549作用,其诱导细胞凋亡可能与钙依赖性通路和MT-1A表达下调有关。

硒化纹党参多糖和其抗A549细胞的活性

目的合成硒化纹党参多糖并探讨其抗人肺腺癌细胞A549的活性。方法以HNO3-Na2Se O3方法硒化纹党参多糖,在单因素试验的基础上,以反应时间、反应温度、纹党参多糖与亚硒酸钠投料比为三因素进行L9(34)正交试验设计,选择硒化纹党参多糖含硒量、产率以及对A549细胞生长的抑制率作为考察指标,优选最佳硒化工艺。结果纹党参多糖的最佳硒化条件为反应时间5 h,反应温度60℃,投料比1∶1。在此条件下,硒化纹党参多糖中含硒量可达1.07 mg/g(RSD为3.7%),产率可达50.3%(RSD为2.5%),对A549细胞的抑制率可达到49.36%(RSD为2.8%)。结论硒化纹党参多糖可以作为抗肿瘤候选药物。

苦参碱诱导肺腺癌A549细胞凋亡及对人端粒酶逆转录酶表达的影响

目的观察苦参碱诱导肺腺癌A549细胞凋亡及对人端粒酶逆转录酶(hTERT)基因表达的影响。方法以终质量浓度为0.1、0.2、0.4、0.6 mg/mL的苦参碱作用肺腺癌A549细胞48 h后,通过台盼蓝拒染法计数细胞的生长抑制率;以终质量浓度为0.2 mg/mL的苦参碱作用A549细胞48、72、96 h后,经透射电镜和DNA Ladder实验了解到细胞凋亡的发生,PCR-TRAP法检测端粒酶活性,实时RT-PCR检测hTERT的mRNA表达水平。结果各种质量浓度的苦参碱作用A549细胞48 h后,均显著抑制细胞的增殖且呈浓度依赖性;0.2 mg/mL的苦参碱作用A549细胞不同时间后,经透射电镜形态学检测和DNA Ladder实验,均显示A549细胞发生了凋亡改变;0.2 mg/mL的苦参碱作用A549细胞48 h后,端粒酶活性明显受抑,hTERT mRNA表达显著降低。结论苦参碱能抑制肺腺癌A549细胞的生长并诱导其凋亡,其机制可能与下调hTERT基因表达,抑制端粒酶活性,破坏端粒稳定性有关。

杨梅树皮提取物体外抗人肺腺癌A549作用的实验研究

目的：分离筛选出杨梅树皮中具有抗人肺腺癌A549的有效部位。方法：采用系统溶剂提取分离法,从杨梅树皮中分离出有效成分,通过~3H-TdR掺入法观察各提取物体外对A549细胞的抑制作用,确定抑瘤效果最好杨梅树皮提取物。结果：各杨梅树皮提取物对A549细胞均有很好的抑制作用,其中杨梅树皮醇提取物和氯仿萃取层部位对人肺腺癌A549的抑制作用最明显,抑制率分别为3.5%～97.0%、38.7%～99.4%,并且具有较好的量效关系。结论：杨梅树皮提取物体外对人肺腺癌A549具有很好的抑制作用。

淫羊藿苷抑制PI3K/AKT通路对肺腺癌A549细胞存活和转移的影响

目的:探讨淫羊藿苷对肺腺癌A549细胞存活和转移的影响及作用机制。方法:CCK8法检测不同浓度淫羊藿苷(0、0.1、0.25、0.5、1、2.5、5、10、20、50、100、200、300和400μmol/L)处理A549细胞后对其存活率的影响,并选择最佳浓度进行后续实验。流式细胞术检测细胞凋亡,划痕实验检测细胞迁移能力,Transwell检测细胞侵袭能力,Western blot法检测上皮标记蛋白E-cadherin和间质标记蛋白N-cadherin、Vimetin表达及PI3K和AKT的磷酸化情况;检测单独或联合给予10μmol/L PI3K激活剂740Y-P对细胞增殖、凋亡、侵袭、迁移和通路蛋白表达的影响。结果:100μmol/L及以上浓度的淫羊藿苷对A549细胞有明显的细胞毒性(P<0.05),选取10、20、50μmol/L作为后续实验浓度;淫羊藿苷可剂量依赖性提高A549细胞凋亡率(P<0.05),抑制细胞侵袭、迁移(P<0.05),影响N-cadherin、E-cadherin和Vimentin蛋白表达(P<0.05),下调PI3K和AKT磷酸化水平可减弱740Y-P对A549细胞增殖、侵袭迁移能力的增强作用,增强其对凋亡的抑制作用。结论:淫羊藿苷可通过影响PI3K/AKT信号通路激活抑制A549细胞存活和转移。

姜黄素对A549细胞亚群SP和NON-SP的NF-κB、VEGF及Notch通路的影响

[目的]通过动物实验了解姜黄提取物-姜黄素抗肿瘤血管生成的具体作用机制。[方法]将40只BALB/C雄性裸小鼠分为4组,每组10只。分别为A组(SP亚群细胞姜黄素组)、B组(SP亚群细胞荷瘤对照组)、C组(NONSP亚群细胞姜黄素组)、D组(NON-SP亚群细胞荷瘤对照组)。A、B两组于实验前建立肺腺癌A549 SP细胞亚群荷瘤模型,C、D两组建立肺腺癌A549 NON-SP细胞亚群荷瘤模型,建立模型后观察16 d,于A组、C组小鼠腹腔注射姜黄素,隔天1次,B、D两组注射生理盐水。16 d后将小鼠称重后处死,剥离瘤块组织,比较各组瘤质量;免疫组化法检测肿瘤组织中血管生长因子(VEGF)、核因子-κB(NF-κB)的表达;逆转录-聚合酶链反应(RT-PCR)检测Notch1 m RNA含量。[结果]肺腺癌A549 SP细胞亚群荷瘤模型组小鼠瘤体与NON-SP细胞亚群荷瘤模型组小鼠相比体积较大;SP亚群细胞姜黄素组抑瘤作用及抗肿瘤血管生成优于NON-SP亚群细胞姜黄素组,两组相比差异具有统计学意义。[结论]姜黄素可以抑制肿瘤生长,考虑可能与其抑制NF-k B的表达,下调Notch1 m RNA含量,阻断Notch信号通路,抑制肿瘤组织中VEGF的表达有关。

全反式维甲酸抑制人肺腺癌A549细胞迁移的机制探讨

目的探讨全反式维甲酸(ATRA)对人肺腺癌细胞迁移的影响及其作用机制。方法细胞划痕实验检测ATRA对A549细胞迁移的影响;Western blot分析肌球蛋白轻链激酶(MLCK)的表达和肌球蛋白轻链(MLC)磷酸化程度;观察MLCK抑制剂ML-7是否影响A549细胞的迁移能力。结果 1 mg.L-1 ATRA处理的A549细胞和细胞对照以及溶剂对照细胞相比,细胞的迁移距离无明显变化,而10 mg.L-1ATRA可明显降低细胞的迁移距离(P<0.05)。Western blot分析结果表明10 mg.L-1 ATRA可明显降低A549细胞ML-CK的表达和MLC磷酸化(P<0.05);ML-7可明显降低A549细胞迁移(P<0.05)。结论 ATRA通过降低MLCK的表达和MLC磷酸化,抑制A549细胞的迁移。

三氧化二砷对人肺腺癌A549/R细胞多药耐药相关蛋白表达的影响

目的探讨三氧化二砷(As2O3)对人肺腺癌A549/R细胞耐药性的逆转作用及对多药耐药相关蛋白(MRP)表达的影响。方法以荧光分光光度计测定细胞内药物浓度的改变,采用半定量逆转录聚合酶联反应(RT-PCR)技术检测As2O3处理后A549/R MRP基因表达的变化。结果As2O3的非细胞毒性剂量可增加A549/R细胞内多柔比星(ADM)浓度,降低其IC50。A549/R细胞中MRP呈过表达状态,不同浓度的As2O3处理A549/R后MRP表达水平明显降低。结论As2O3可部分逆转A549/R细胞对ADM的耐药性,其逆转机制与改变MRP基因表达有关。