8—MOP与ATRA联合应用对Mc3细胞bcl—2和P~(53)表达的影响

目的:研究8—MOP、ATRA以及二者联合应用对Mc3细胞bcl-2和P~(53)表达的影响。方法:免疫组织化学染色方法。结果:bcl—2表达分别为:对照组( );8-MOP组( );ATRA(-);8—MOP与ATRA联合用药组( );P~(53)表达分别为:对照组( );8-MOP组( );ATRA( );8—MOP与ATRA联合用药组( )。结论:①ATRA处理组细胞bcl—2的阳性表达明显下降,可能导致Mc3细胞发生凋亡;②P~(53)的表达无明显变化。     

8—MOP、ATRA以及二者联合应用对Mc3细胞nm—23表达的影响

目的 研究8—MOP、ATRA以及二联合应用对Mc3细胞mm-23基因蛋白表达的影响．方法 采用免疫组织化学染色法。结果 对照组( )．8—MOP组( ),ATRA组( ),8—MOP ATRA组( )。结论 8—MOP、ATRA及二联合应用使Mc3细胞nm—23的阳性表达下降,可能对Mc3细胞的转移特性有影响。     

姜黄素协同阿霉素抑制乳腺癌细胞生长的作用及其机制

目的探讨姜黄素联合阿霉素(adriamycin,ADM)对人乳腺癌MCF-7及MDA-MB-231细胞生长的影响及其作用机制。方法将体外培养的乳腺癌MCF-7及MDA-MB-231细胞处理不同浓度的姜黄素及ADM,MTT法检测细胞成活率,等效剂量法(Calcusy)分析联合指数,然后利用免疫印迹法检测PARP、Bcl-2、Bax及NF-κB(p65)蛋白表达水平。结果姜黄素和ADM两者合用可以协同抑制人乳腺癌MCF-7及MDA-MB-231细胞生长,其联合指数(ED50CI)分别为0.7和0.62。免疫印迹结果显示,联合给药可以明显增强MCF-7细胞PARP蛋白裂解,抑制Bcl-2蛋白表达,但对Bax蛋白表达无明显影响。联合用药可以抑制ADM诱导的NF-κB信号通路激活。结论姜黄素和ADM可能通过抑制ADM诱导的NF-κB激活继而促进肿瘤细胞凋亡来发挥协同的抗乳腺癌作用。     

8—MOP、ATRA以及二者联合应用对Mc3细胞nm-23表达的影响

目的 研究8-MOP、ATRA以及二者联合应用对Mc3细胞um-23基因蛋白表达的影响。方法 采用免疫组织化学染色法。结果 对照组(++),8-MOP组(+),ATRA组(+),8-MOP+ATRA组(+)。结论 8-MOP、ATRA及二者联合应用使Mc3细胞um-23的阳性表达下降,可能对Mc3细胞的转移特性有影响。     

黄荆子乙酸乙酯提取物对人乳癌细胞体内外实验的研究

目的研究黄荆子乙酸乙酯提取物（EVn-50）在体内外对人乳癌MDA—MB-435S细胞的抑制作用。方法软琼脂克隆形成法测定细胞生长：溴化尿嘧啶（BrdU）掺入法检测细胞核酸的合成；建立MDA—MB-435S裸鼠异种移植瘤模型，观察经EVn-50处理后的肿瘤抑制率。结果在体外，随EVn-50浓度增高，细胞集落形成率明显下降（P〈0．01）；EVn-50对MDA—MB-435S细胞核酸合成具有抑制作用，呈剂量依赖性，其中高剂量组的BrdU掺入抑制作用最强，IC50为16．8ug／mL。在体内，EVn-50抑制MDA—MB-435S细胞裸鼠异种移植瘤生长，20、40、80ug／mL的EVn-50对移植瘤的瘤重抑制率分别为18％、31％和63％，呈浓度依赖性。结论EVn-50在体内外对MDA—MB-435S细胞均具有生长抑制作用。     

高效液相色谱分析全反式维甲酸在HL-60细胞液中的含量变化

目的　分析HL - 6 0细胞培养液中全反式维甲酸 (ATRA)的含量变化 ,为临床治疗白血病提供实验依据。方法　急性早幼粒白血病细胞株HL - 6 0 ,经ATRA及联合用药处理。乙醚 -丙酮 (8∶1v/v)提取ATRA ,高效液相色谱法分析。结果　A TRA在 2 .5 0× 10 -2 ～ 1.0 0× 10 μmol·L-1的范围内 ,有良好的线性关系。平均回收率 94 .5 % ,相对标准差小于 4 .0 3%。联合用药各组、各时相点的ATRA的含量均高于ATRA单独处理组 ,其环比显示 :联合用药各组 ,各时相点ATRA的分解比ATRA单独处理组低。结论　联合用药治疗急性早幼粒白血病具有协同作用 ,适于临床应用     

吩噻嗪衍生物协同放射对HeLa细胞增殖的抑制效应比较研究

目的 探讨吩噻嗪衍生物对人宫颈癌HeLa细胞增殖的抑制作用及与放射联合应用抑制肿瘤的协同效应。方法 采用MTT法和细胞克隆形成法检测细胞的增殖活性和细胞辐射敏感性。结果 比较了6种吩噻嗪衍生物对HeLa细胞增殖的抑制效应，发现化合物α-氯-N-二甲胺基乙基吩噻嗪（PTZD2）、α-三氟甲基-N-二甲胺基乙基吩噻嗪（PTZD3）和α-氯-N-二乙胺基乙基吩噻嗪（PTZD5）的作用比较明显，在10μmol／L浓度能产生出显著抑制效应，40-50μmol／L浓度作用3和4d，细胞增殖完全被抑制而死亡。PTZD2或PTZD3与放射联合应用，显示出明显抗HeLa细胞增殖的协同效应，10μmol／L PTZD3对2和4Gy照射细胞的增殖抑制的增强比分别为3．5和1．8。实验结果还表明，在照射前18h用药的协同作用更加显著。结论 吩噻嗪衍生物具有程度不同的抑制HeLa细胞增殖的作用，与放射联合应用具有抗肿瘤的协同效应，而且照射前18h用药的效应最佳。     

外源性机械生长因子对大鼠骨骼肌卫星细胞生物学特性的影响

目的:研究机械生长因子(MGF)促离体培养的骨骼肌卫星细胞增殖的最佳浓度,并观察该浓度对细胞生长曲线、总蛋白及凋亡情况的影响。方法:选用雄性SD大鼠1只,无菌条件下取后肢肌肉,采用改进的两步酶消化法结合差速贴壁技术,分离及纯化骨骼肌卫星细胞。取第3代骨骼肌卫星细胞,分别采用终浓度为15、25、50、100、200 ng/ml的MGF进行干预,作为实验组;另以单纯加入100μl生长培养基作为对照组,以加入100μl DMEM作为阴性对照组。同步化后,于培养24 h后加入CCK-8溶液。采用CCK-8比色法检测不同浓度MGF下细胞的增殖情况并筛选出最佳浓度后,绘制生长曲线,同时运用BCA法及Hoechst 33342、PI双染法测定最佳增殖浓度的MGF对卫星细胞蛋白合成及细胞凋亡的影响。免疫细胞化学法鉴定骨骼肌卫星细胞。结果:①终浓度为15、25、50、100 ng/ml的MGF均有促进骨骼肌卫星细胞增殖的作用(P<0.01),其中25 ng/ml MGF促增殖作用最佳。②与对照组相比,MGF组细胞生长曲线左移,倍增时间、平台期均缩短。③与对照组相比,25 ng/ml MGF作用48 h即对骨骼肌卫星细胞有明显的增殖效果(P<0.05);与对照组相比,25 ng/ml MGF作用骨骼肌卫星细胞48 h和72 h时,其总蛋白含量显著增加(P<0.05);与对照组相比,25 ng/ml MGF作用72h、96h,骨骼肌卫星细胞的平均凋亡指数显著减小(P<0.05)。结论:①机械生长因子可促进体外培养的大鼠骨骼肌卫星细胞增殖,最佳浓度为25 ng/ml;②25 ng/ml MGF可以使骨骼肌卫星细胞提前进入平台期,缩短生长周期;③25 ng/ml MGF可以抑制骨骼肌卫星细胞的凋亡。     

17β-雌二醇对人涎腺黏液表皮样癌Mc3增殖周期的影响

目的 探讨17β-雌二醇(E2)对体外培养的人涎腺黏液表皮样癌Mc3细胞系增殖周期的影响。方法 以不同浓度、时间的E2处理Mc3细胞,采用MTT法、流式细胞术、免疫组织化学染色法,检测E2对人涎腺黏液表皮样癌Mc3细胞系细胞群体倍增时间、细胞周期分布以及对CyclinDl、P27^Kip1阳性表达的影响。结果 浓度分别为10^-9、10^-8、10^-7mol／L的E2作用于细胞第5天时,MTT法测得E2处理组细胞增殖促进率分别为29％、54％、59％,CyclinDl的阳性表达率分别增加了16％、9％、24％,P27^Kip1。的阳性表达率分别减少了33％、30％、55％。流式细胞术检查结果显示,10^-7mol／L的E2处理12、18、24h后,细胞周期中S期细胞比相应对照组分别增加了11．3％、6．6％、46．7％,细胞增殖指数分别增加了6．0％、3．6％、205．5％。结论 生理浓度的E2可以促进CyclinD1的表达、降低．P27^Kip1的阳性表达,从而促进细胞周期Gη／s期转换,增加S期细胞数量,加速DNA合成,刺激肿瘤发生、发展。     

全反式维甲酸对乳腺癌MCF-7细胞周期和增殖活性的影响及restin基因表达的初步研究

目的:检测全反式维甲酸(all-trans retinoic acid,ATRA)在乳腺癌MCF-7细胞周期、增殖、分化和凋亡过程中的作用,以及对。restin基因表达的影响,从而为研究其功能提供线索。方法:用流式细胞仪(FCM)检测细胞周期的变化;MTT 法检测细胞增殖活性;RT-PCR检测restin基因表达。结果:在ATRA诱导下,细胞出现G1期阻滞和生长抑制,增殖活性下降,restin基因开始表达,并呈增长趋势。结论:在ATRA诱导MCF-7细胞分化、凋亡过程中,ATRA能使MCF-7细胞 G1期阻滞,并能抑制MCF-7细胞生长,促使其凋亡,restin基因参与细胞周期的调控,特别是细胞凋亡。     

1H NMR visible lipids are induced by phosphonium salts and 5-fluorouracil in human breast cancer cells.

Cationic lipophilic phosphonium salts (CLPS) selectively accumulate in the mitochondria of neoplastic cells and inhibit mitochondrial function. The effects of the CLPS p-(triphenylphosphoniummethyl) benzaldehyde chloride (drug A), and [4-(hydrazinocarboxy)-1-butyl] tris-(4-dimethylaminophenyl) phosphonium chloride (drug B), on human breast cells of differing biological properties were assessed using growth inhibition assays and 1H NMR. Drug A and, to a lesser extent, drug B demonstrated selective growth inhibition of the highly tumorigenic DU4475 breast carcinoma cell line compared to the transformed HBL-100 human breast cell line. However, in contrast to previous studies using other cell lines, no synergistic activity was found when the drugs were used in combination. 1H NMR demonstrated significant increases in mobile lipid acyl chain resonances in both cell lines treated with cytotoxic doses (IC50, 48 h) of the drugs used either alone or in combination. Two-dimensional NMR revealed accompanying decreases in phosphocholine/Lys levels in HBL-100 cells treated with A, B, or a 1:1 combination A+B at the IC50, and in DU4475 cells treated with drug A (IC50). This was accompanied by significant increases in cho/Lys ratios with IC50 A or combination A+B treatment. Similar spectra were observed in cells treated with 5-fluorouracil but not methotrexate, indicating that mobile lipid accumulation is a general but not universal response to cytotoxic insult.     

雷公藤红素联合5-氟尿嘧啶在人结肠癌细胞中的相互作用

目的体外观察雷公藤红素与5-氟尿嘧啶（5-FU）联用在人结肠癌HCT-116细胞增殖中的相互作用。方法采用MTT法观察不同浓度雷公藤红素及5-FU单独或联合应用对结肠癌细胞的生长抑制作用,并利用中效原理判断联合用药的效果。结果雷公藤红素和5-FU单独应用时,随药物浓度增加对HCT-116细胞的抑制作用也增加,中效浓度分别为3.533μmol/L,9.254μmol/L,两药联用时在大部分效应范围（0〈fa〈83％）表现协同作用（CI〈1），中效浓度为6．433μmol／L．其中雷公藤红素0．099μmol／L，5-FU6．33μmol／L。两药合用给药时间及次序不同时不同时，合用效应无明显差异。结论上述两种药物联合应用时具有较好的协同效应，且药物效应与给药顺序无关。     

Enhanced expression of adenovirus-mediated sodium iodide symporter gene in MCF-7 breast cancer cells with retinoic acid treatment.

Increased expression of the sodium iodide symporter (NIS) is required for effective radioiodine treatment and reporter gene imaging of breast cancer. We investigated the effect of retinoic acid on adenovirus-mediated expression of the human NIS gene in the MCF-7 breast cancer cell line. METHODS: The MCF-7 cell line was infected with recombinant adenovirus carrying the human NIS gene (Rad-NIS). Levels of NIS messenger RNA (mRNA) and protein expression and radioiodine ((125)I) uptake were measured to evaluate adenovirus-mediated NIS gene expression in wild-type and Rad-NIS-infected MCF-7 cells after treatment with all-trans-retinoic acid (ATRA; 10(-8)-10(-6) mol/L). RESULTS: The transduction efficiency of adenovirus in MCF-7 cells at a multiplicity of infection (MOI) of 50 was >60%. After incubation with 10(-6) mol/L ATRA, the mRNA level in Rad-NIS-infected MCF-7 cells increased to 118.5 times that of wild-type MCF-7 cells, whereas the mRNA level in wild-type MCF-7 cells showed only a 2.1-fold increase. Western blot, immunocytochemical staining, and flow cytometry analyses showed that NIS protein expression in MCF-7 cells infected with Rad-NIS increased after ATRA treatment. With ATRA treatment, the amount of (125)I uptake increased in a dose-dependent manner (P < 0.001). The (125)I uptake in wild-type MCF-7 cells increased 3.1-, 5.5-, and 7.6-fold with treatment with 10(-8), 10(-7), and 10(-6) mol/L ATRA, respectively. Rad-NIS-infected cells showed a 4.0-fold increase in (125)I uptake. Treatment of Rad-NIS-infected cells with 10(-8), 10(-7), and 10(-6) mol/L ATRA increased (125)I uptake by 4.9-, 8.2-, and 27.6-fold, respectively, compared with wild-type MCF-7 cells. The level of NIS expression in Rad-NIS-infected MCF-7 cells treated with 10(-6) mol/L ATRA (245.0 +/- 13.7 pmol/10(6) cells) was much greater than the sum of the expression levels seen in ATRA-treated wild-type cells and Rad-NIS-infected wild-type cells. CONCLUSION: Retinoic acid increases adenovirus-mediated NIS expression in MCF-7 cells. Our results indicate that improved efficiency of NIS gene therapy or reporter imaging in breast cancer may be possible with retinoic acid treatment.     

全反式维甲酸联合丁酸甘油酯诱导滤泡状甲状腺癌的实验研究

目的 探讨全反式维甲酸(ATRA)联合丁酸甘油酯(TB)诱导滤泡状甲状腺癌细胞株FTC-133钠/碘同向转运体(NIS)和甲状腺球蛋白(Tg)表达及其碘的摄取.方法 单独使用1 μmol/LATRA或0.1,0.25,0.5,1 mmol/L TB和联合使用该2种药物诱导FTC-133 48 h后,用实时定量PCR反应检测NIS mRNA和Tg mRNA的表达,蛋白印迹法检测NIS蛋白表达,放射免疫法检测Tg蛋白含量以及检测FTC-133诱导后摄碘变化.结果 TB可诱导FTC-133 NIS、Tg蛋白及mRNA的表达增高,并呈剂量依赖性.联合1 μmol/L ATRA及各浓度TB后较单独使用1 μmol/L ATRA及TB明显提高了FTC-133 NIS、Tg蛋白及mRNA的表达,并且增加了FTC.133对125I的摄取.结论 ATRA联合TB有效增强了FFC-133的摄碘能力,为低分化甲状腺癌的放射性碘治疗提供了一条新的研究途径.     

8－氮鸟嘌呤诱变3D_5杂交瘤细胞的初步研究

小鼠杂交瘤３Ｄ５为一株分泌抗人红细胞非凝集性单克隆抗体的杂交瘤细胞株，用８－氮鸟嘌呤（８－ＡＧ）诱变处理可以使之成为具有模拟骨髓瘤性质的次黄嘌呤鸟嘌呤磷酸核糖转移酶缺失的杂交瘤细胞系，并且保留杂交瘤细胞系分泌抗体的能力，在利用自身血细胞凝集试验对各种病原体的快速诊断中应用广泛。实验表明，用不同剂量的８－ＡＧ进行诱变，在不同剂量水平上３Ｄ５杂交瘤细胞主要呈现细胞生长抑制、部分细胞衰老死亡、存活细胞分裂生长成为多细胞克隆及细胞适应８－ＡＧ诱变后恢复正常生长能力等一系列的变化过程。利用间接免疫荧光方法检测３Ｄ５分泌抗体结果表明，诱变后３Ｄ５杂交瘤细胞株仍然保持有分泌抗人红细胞非凝集性单克隆抗体的能力，此细胞系的建立不仅为研制自身血细胞凝集试验的双功能抗体奠定了基础，同时也具有一定理论意义     

2004 Dr. Gary J. Becker Young Investigator Award: Relative thermosensitivity of cytotoxic drugs used in transcatheter arterial chemoembolization

PURPOSE: Large hepatocellular carcinoma tumors are being treated increasingly with a combination of transcatheter arterial chemoembolization (TACE) and radiofrequency (RF) ablation. However, the high temperatures reached during RF ablation may reduce the cytotoxic effects of antineoplastic agents, but this has not been studied. Therefore, in the present study, the relative thermosensitivity of cytotoxic drugs commonly used in TACE was studied.MATERIALS AND METHODS: The relative cytotoxic effects of cisplatin, doxorubicin HCl, and mitomycin on the growth of human colon HT29 and lung A549 adenocarcinoma cells before and after heating each drug in solution was determined from the standpoints of different durations of exposure (15, 30, 60, 90, and 120 minutes) at a fixed temperature (120 degrees C) and exposure to different temperatures (60 degrees C, 80 degrees C, 100 degrees C, and 120 degrees C) for a fixed period of time (2 hours). After 72 hours of exposure of the cells to each drug, relative cell growth inhibition was assessed by MTT assay, and 50% inhibitory concentration (IC(50)) values were calculated for each cytotoxic agent. Finally, the heat-dependent degradation of mitomycin and doxorubicin was analyzed with use of tandem electrospray mass spectrometry. RESULTS: The relative cytotoxic activities (shown by cell growth inhibition and IC(50) values) of cisplatin, doxorubicin, and mitomycin heated to 120 degrees C for 2 hours decreased by factors of 1.35 (range, 1-1.75), 9.5 (range, 8.5-10.5), and 7.05 (range, 3.5-12), respectively. The cytotoxic activities of doxorubicin and mitomycin continued to decrease with incremental increases in temperature. Similarly, with incremental increases in the duration of exposure to heat, the cytotoxic activities of doxorubicin and mitomycin decreased. Mass spectrometric analysis of residual drug content showed that a 2-hour exposure to a temperature of 120 degrees C caused doxorubicin and mitomycin to degrade by 95% and 84%, respectively. CONCLUSIONS: The cytotoxicity of cisplatin is not affected by heat. The cytotoxicities of doxorubicin and mitomycin are reduced by high temperature and duration of exposure to heat. Although degradation of cytotoxicity starts at 60 degrees C and after 30 minutes of exposure to heat, statistically significant changes are encountered at 100 degrees C and after 90 minutes of exposure.     

Irradiation and Various Cytotoxic Drugs Enhance Tyrosine Phosphorylation and β1-Integrin Clustering in Human A549 Lung Cancer Cells in a Substratum-Dependent Manner in Vitro

BACKGROUND AND PURPOSE: Interactions of cells with a substratum, especially extracellular matrix proteins, initiate clustering of integrin receptors in the cell membrane. This process represents the initial step for the activation of signaling pathways regulating survival, proliferation, differentiation, adhesion, and migration, and could, furthermore, be important for cellular resistance mediating mechanisms against radiation or cytotoxic drugs. The lack of data elucidating the impact of irradiation or cytotoxic drugs on this important phenomenon led to this study on human A549 lung cancer cells in vitro. MATERIAL AND METHODS: The human lung carcinoma cell line A549 grown on polystyrene or fibronectin (FN) was irradiated with 0-8 Gy or treated with cisplatin (0.1-50 microM), paclitaxel (0.1-50 nM), or mitomycin (0.1-50 microM). Colony formation assays, immunofluorescence staining in combination with activation of integrin clustering using anti-beta(1)-integrin antibodies (K20), and Western blotting for tyrosine phosphorylation under treatment of cells with the IC(50) for irradiation (2 Gy; IC(50) = 2.2 Gy), cisplatin (2 microM), paclitaxel (5 nM), or mitomycin (7 microM) were performed. RESULTS: Attachment of cells to FN resulted in a significantly reduced radio- and chemosensitivity compared to polystyrene. The clustering of beta(1)-integrins examined by immunofluorescence staining was only stimulated by irradiation, cisplatin, paclitaxel, or mitomycin in case of cell attachment to FN. By contrast, tyrosine phosphorylation, as one of the major events following beta(1)-integrin clustering, showed a 3.7-fold, FN-related enhancement, and treatment of cells with the IC(50) of radiation, cisplatin, paclitaxel, or mitomycin showed a substratum-dependent induction. CONCLUSION: For the first time, a strong influence of irradiation and a variety of cytotoxic drugs on the clustering of beta(1)-integrins could be shown. This event is a prerequisite for tyrosine phosphorylation and, thus, the activation of cellular mechanisms regulating survival, proliferation, and adhesion. These data are not only important for the understanding of cellular resistance against cytotoxic agents but, furthermore, for tumor progression, anchorage-independent cell growth, and, possibly, the optimization of radiochemotherapeutic strategies.     

Evaluation of the Hsp90 inhibitor NVP-AUY922 in multicellular tumour spheroids with respect to effects on growth and PET tracer uptake

BackgroundMolecular targeting has become a prominent concept in cancer treatment and heat shock protein 90 (Hsp90) inhibitors are suggested as promising anticancer drugs. The Hsp90 complex is one of the chaperones that facilitate the refolding of unfolded or misfolded proteins and plays a role for key oncogenic proteins such as Her2, Raf-1, Akt/PKB, and mutant p53. NVP-AUY922 is a novel low-molecular Hsp90 inhibitor, currently under clinical development as an anticancer drug. Disruption of the Hsp90-client protein complexes leads to proteasome-mediated degradation of client proteins and cell death.The aim of the current study was to use a combination of the multicellular tumour spheroid (MTS) model and positron emission tomography (PET) to investigate the effects of NVP-AUY922 on tumour growth and its relation to PET tracer uptake for the selection of appropriate PET tracer. A further aim was to evaluate the concentration and time dependence in the relation between growth inhibition and PET tracer uptake as part of translational imaging activities.MethodsMTS of two breast cancer cell lines (MCF-7 and BT474), one glioblastoma cell line (U87MG) and one colon carcinoma cell line (HCT116) were prepared.Initially, we investigated MTS growth pattern and ³H-thymidine incorporation in MTS after continuous exposure to NVP-AUY922 in order to determine dose response. Then the short-term effect of the drug on the four PET tracers 2-[¹⁸F] fluoro-2-deoxyglucose (FDG), 3′-deoxy-3′-fluorothymidine (FLT), methionine and choline was correlated to the long-term effect (changes in growth pattern) to determine the adequate PET tracer with high predictability.Next, the growth inhibitory effect of different dose schedules was evaluated to determine the optimal dose and time. Finally, the effect of a 2-h exposure to the drug on growth pattern and FDG/FLT uptake was evaluated.ResultsA dose-dependent inhibition of growth and decrease of ³H-thymidine uptake was observed with 100% growth cessation in the dose range 7–52 nM and 50% ³H-thymidine reduction in the range of 10–23 nM, with the most pronounced effect on BT474 cells.The effect of the drug was best detected by FLT. The results suggested that a complete cessation of growth of the viable cell volume was achieved with about 50% inhibition of FLT uptake 3 days after continuous treatment.Significant growth inhibition was observed at all doses and all exposure time spans. Two-hour exposure to NVP-AUY922 generated a growth inhibition which persisted dose dependently up to 10 days. The uptake of FDG per viable tumour volume was reduced by just 25% with 300 nM treatment of the drug, whereas the FLT uptake decreased up to 75% in correlation with the growth inhibition and recovery.ConclusionsOur results indicate a prolonged action of NVP-AUY922 in this cell culture, FLT is a suitable tracer for the monitoring of the effect and a FLT PET study within 3 days after treatment can predict the treatment outcome in this model. If relevant in vivo, this information can be used for efficient planning of animal PET studies and later human PET trial.     

LM-1685对人肺腺癌细胞A549的放射增敏作用

目的 观察环氧合酶-2(COX-2)抑制剂对肺癌细胞的放射增敏作用。方法COX-2抑制剂LM-1685作用于体外培养的肺癌细胞A549,噻唑蓝(MTT)法检测其对肺癌细胞的抑制效果,克隆形成法检测放射敏感性,流式细胞术检测细胞周期变化。结果COX-2抑制剂LM-1685具有明显的抑制A549细胞增殖的作用,其效应呈时间和剂量依赖性,50 μmol/L LM-1685在有或没有IL-1β作用下对A549细胞均有放射增敏作用,其放射增敏比分别为1.12、1.06。50 μmol/L LM-1685能去除X射线导致的A549细胞G₂/M期阻滞。结论COX-2抑制剂对肺癌细胞A549具有放射增敏作用,放射增敏机制可能与去除G₂/M期阻滞有关。