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1.
目的 探究白屈菜红碱(CHE)对腺样囊性癌细胞(ACC2)生长的抑制作用及机制。方法 利用CCK8法、EdU法、Hoechst33342/PI双染色法、试剂盒法检测CHE对ACC2细胞活力、细胞增殖、细胞凋亡和活性氧(ROS)水平的影响;通过Western blotting技术检测CHE对Cleaved-Caspase 3、PARP、NF-κB、p-JNK、p-p38蛋白表达的影响;利用斑马鱼移植瘤模型检测CHE对斑马鱼体内ACC2细胞生长的抑制作用。结果 CCK-8结果显示:与对照组比较,2、3、4、5、6、7、8、9、10 μmol/L的CHE显著降低ACC2细胞的存活率(P<0.05、0.01),且呈浓度相关性; ROS检测结果显示:与对照组比较,5、8 μmol/L的CHE导致ACC2细胞内的ROS水平显著上升(P<0.05、0.01); EdU增殖检测结果表明:与对照组比较,5、8 μmol/L的CHE致使ACC2细胞的增殖能力显著下降(P<0.01);Hoechst/PI染色结果显示:与对照组比较,CHE 5、8 μmol/L组ACC2细胞凋亡率显著上升(P<0.01)。抗氧化剂N-乙酰半胱氨酸(NAC)显著抑制CHE诱导的ROS水平升高、细胞凋亡增加(P<0.01);Western blotting结果显示:2、5、8 μmol/L的CHE能够显著上调Cleaved-Caspase 3、PARP、NF-κB蛋白的表达(P<0.01),且呈现浓度相关性,5、8 μmol/L的CHE能够显著上调p-JNK的蛋白表达(P<0.01),8 μmol/L的CHE能够显著上调p-p38的蛋白表达(P<0.01);NAC显著降低由CHE导致的Cleaved-Caspase 3、PARP、NF-κB、p-JNK、p-p38蛋白表达增加(P<0.01),5、8 μmol/L CHE能够有效抑制斑马鱼体内肿瘤的生长(P<0.01)。结论 体外及斑马鱼移植瘤模型证明,CHE可以有效抑制ACC2细胞生长,其机制与提高细胞ROS水平,上调NF-κB、p-JNK、p-p38表达,从而抑制细胞增殖、诱导细胞凋亡相关。 相似文献
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目的 探讨miR-578调控长链脂酰辅酶A合成酶4(ACSL4)对胃癌细胞增殖及侵袭的影响。方法 选取人胃癌细胞MKN-45、SNU-1、MKN-7、KTAO3、N87及人正常胃黏膜细胞GES-1为研究对象,将MKN-45细胞分为对照组、miR-578 NC组、miR-578 mimic组、miR-578 mimic+pc-ACSL4组,测定各组MKN-45细胞活力及凋亡、侵袭、迁移能力,测定细胞中miR-578、ACSL4、凋亡相关蛋白(Bax、Caspase-3、Bcl-2)、侵袭相关蛋白(MMP-9、MMP-2)的表达,验证miR-578与ACSL4的靶向关系。结果 miR-578在人胃癌细胞中低表达;与对照组相比,miR-578 mimic组MKN-45细胞活力、侵袭、迁移能力、MMP-2、MMP-9、Bcl-2蛋白表达水平均显著降低(P<0.05),凋亡能力、Caspase-3、Bax蛋白表达水平均显著升高(P<0.05);与miR-578 mimic组相比,miR-578 mimic+pc-ACSL4组MKN-45细胞活力、侵袭、迁移能力、MMP-2、MMP-9、Bcl-2蛋白表达水平均显著升高(P<0.05),凋亡能力、Caspase-3、Bax蛋白表达水平均显著降低(P<0.05);荧光素酶实验结果显示,miR-578与ACSL4存在靶向调节关系。结论 miR-578可抑制人胃癌细胞MKN-45的增殖及迁移能力,可能是通过抑制ACSL4表达实现的。 相似文献
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目的 探讨羌活醇及异欧前胡素对大鼠成纤维样滑膜细胞增殖抑制的影响。方法 复制经脂多糖(LPS)诱导的大鼠成纤维样滑膜细胞(CIA-FLS)模型,分别给予不同浓度的羌活醇(25、50、100、200、400 μg·mL-1)、异欧前胡素(25、50、100、200、400 μg·mL-1)及阳性药泼尼松龙(400 μg·mL-1),另设空白对照组,观察给药前后成纤维样滑膜细胞形态差异;采用噻唑蓝(MTT)法测定不同给药时间、不同给药浓度下成纤维样滑膜细胞的抑制率,计算半数抑制浓度(IC50);硝酸还原酶法测定羌活醇和异欧前胡素对大鼠成纤维化滑膜细胞中一氧化氮(NO)水平的影响;ELISA测定肿瘤坏死因子a (TNF-a)表达的影响。结果 造模细胞较正常细胞增殖力强,细胞粗大,纤维样,呈层叠状生长;羌活醇组给药后细胞增殖力减弱,生长良好;异欧前胡素给药后细胞增殖力锐减,生长状况不佳。给药12 h,羌活醇未测出半数抑制浓度值,异欧前胡素半数抑制浓度值为160 μg·mL-1;给药36 h,羌活醇、异欧前胡素半数抑制浓度值分别为190、120 μg·mL-1;给药60 h,分别为80、45 μg·mL-1,异欧前胡素的增殖抑制能力强于羌活醇(P<0.01)。给药羌活醇与异欧前胡素对一氧化氮总体含量和细胞因子肿瘤坏死因子a含量均有显著性降低(P<0.01),且异欧前胡素的降低更显著。结论 羌活醇及异欧前胡素对大鼠成纤维样滑膜细胞均有增殖抑制作用(P<0.05),均使一氧化氮含量和细胞因子TNF-a的含量显著减少(P<0.01),二者都有很好的增殖抑制能力,且异欧前胡素的抑制效果优于羌活醇。 相似文献
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目的 研究五味子乙素对H2O2诱导小神经胶质BV-2细胞氧化应激损伤的保护作用,并探讨其可能的作用机制。方法 体外常规培养BV-2细胞,用H2O2诱导细胞氧化应激损伤模型,将细胞分为正常对照组、模型组、五味子乙素10,20,40 μmol·L-1组。CCK8试剂盒检测五味子乙素对细胞存活率的影响,相关试剂盒检测细胞匀浆中MDA、NO含量及SOD活性,免疫印迹方法检测Jak2、p-Jak2、State3、p-State3、HO-1及SOD1蛋白表达水平。结果 与模型组相比,不同剂量的五味子乙素可明显增加细胞的存活率、降低氧化应激产物MDA及NO的释放、增强SOD酶活性,差异均有统计学意义(P<0.05);免疫印迹结果显示五味子乙素可明显提高HO-1、SOD1蛋白水平,并抑制Jak2、State3的磷酸化水平,与模型组相比差异有统计学意义(P<0.05)。结论 五味子乙素可明显降低BV-2细胞的氧化应激损伤,其作用机制可能与抑制Jak2/State3信号通路的活化有关。 相似文献
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目的 研究白花丹醌在缺氧条件下对人肝癌细胞HepG2增殖、凋亡、侵袭和低氧诱导因子1α(hypoxia induced factor1α,HIF-1α)及其下游基因表达的影响。方法 采用二氯化钴(CoCl2)化学诱导法建立HepG2细胞体外缺氧模型,经不同浓度(2,4,8 μmol·L–1)白花丹醌处理24 h后,MTT、平板克隆形成试验观察HepG2细胞增殖水平变化;使用Annexin V/PI双染流式细胞术检测HepG2细胞凋亡情况;使用Transwell试验观察HepG2细胞侵袭能力的变化;使用qRT-PCR检测HepG2细胞内HIF-1A mRNA转录水平变化;使用Western blotting检测细胞内HIF-1α及其下游基因c-Myc、VEGFA、MMP9和TWIST1的蛋白表达水平。结果 当CoCl2处理浓度为150 μmol·L–1时,HepG2细胞增殖水平未见显著变化,而HIF-1α蛋白表达水平显著升高(P<0.01),提示体外缺氧模型建立成功。与常氧对照组相比,MTT、平板克隆形成试验结果显示不同浓度白花丹醌作用HepG2细胞后,其增殖水平受到显著抑制(P<0.05或P<0.01); Transwell试验结果显示白花丹醌可显著抑制HepG2细胞侵袭(P<0.05或P<0.01);流式细胞术结果表明白花丹醌能显著诱导HepG2细胞凋亡(P<0.05或P<0.01);Western blotting及qRT-PCR检测结果显示,白花丹醌能显著下调HIF-1α蛋白及HIF-1A mRNA表达水平(P<0.05或P<0.01)。Western blotting检测结果显示HIF-1α及其下游基因c-Myc、VEGFA、MMP9和TWIST1的蛋白表达水平均显著下调(P<0.05或P<0.01)。结论 CoCl2体外模拟肝癌HepG2细胞缺氧的适宜浓度为150 μmol·L–1;在缺氧条件下,白花丹醌可显著抑制肝癌HepG2细胞的增殖与侵袭,同时诱导细胞凋亡,其作用机制可能与下调HIF-1α蛋白及其下游靶基因蛋白表达有关。 相似文献
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槲皮素诱导人结肠癌细胞HT-29凋亡的机制研究 总被引:1,自引:1,他引:0
目的 探讨槲皮素在体外对人结肠癌HT-29细胞凋亡的影响,并对其诱导机制进行研究。方法 体外常规培养HT-29细胞,随机设定对照组和高、中、低剂量(32,16,8 μg·mL-1)槲皮素组,药物干预24 h后,采用CCK-8试剂盒检测槲皮素对HT-29细胞增殖的影响,倒置显微镜观察细胞形态变化,蛋白免疫印迹法检测MKK3/6/p38信号通路蛋白表达,并同时检测凋亡相关蛋白Caspase 8、Caspase 3、Bax及Bcl-2的表达水平。结果 槲皮素干扰HT-29细胞24 h后,CCK-8实验发现槲皮素可明显抑制细胞的增殖;形态学观察发现细胞密度明显减小、细胞体积变小;免疫印迹实验发现槲皮素可诱导MKK3/6及p38的磷酸化,进而促进促凋亡蛋白Caspase8、Caspase3及Bax的表达,抑制了抗凋亡蛋白Bcl-2的表达。结论 槲皮素可诱导人结肠癌HT-29细胞凋亡,其作用机制可能与激活MKK3/6/p38信号通路有关。 相似文献
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目的 观察龙胆苦苷对血管平滑肌细胞(vascular smooth muscle cells,VSMC)增殖、迁移能力的影响,并探讨其可能的作用机制。方法 体外分离培养大鼠血管平滑肌细胞,将血管平滑肌细胞随机分为分为control组、GPS处理组、PF-3758309+GPS组。采用噻唑蓝(MTT)法观察各组细胞增殖能力,计算细胞增殖抑制率;采用细胞划痕实验观察各组细胞迁移能力,计算细胞迁移率。采用Western blotting法检测各组细胞Pak4及MMP-2表达情况。结果 与对照组相比,龙胆苦苷处理组细胞增殖率及迁移率明显降低(P<0.01),GPS组细胞内Pak4、MMP-2 表达水平明显降低(P<0.01);而与GPS组相比,PF-3758309+GPS组可明显增加细胞增殖率及迁移率(P<0.05),血管平滑肌细胞内 MMP-2 表达水平明显上调(P<0.05)。 结论 龙胆苦苷具有抑制血管平滑肌细胞增殖及迁移,其机制可能与抑制Pak4相关。 相似文献
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目的 探讨白藜芦醇对肺癌细胞生长活性的抑制效应及可能的机制。方法 稳定培养肺癌细胞系H292,分别加入含10、20、40 μmol·L-1白藜芦醇的培养基进行干预,采用CCK-8、流式细胞术、细胞集落形成实验检测白芦藜醇对H292细胞生长活性的影响,采用免疫荧光、Western blotting检测白藜芦醇对细胞Akt/mTOR信号通路相关蛋白的影响。结果 (1) CCK-8检测结果显示,白藜芦醇对H292细胞增殖有明显抑制作用(P<0.05),且呈时间和剂量依赖性,同时对H292细胞周期有明显影响,能阻滞细胞周期于G2/M期。(2)白藜芦醇可明显抑制H292细胞集落形成(P<0.05),并呈剂量依赖性。(3) Western blotting检测结果显示,白藜芦醇以剂量依赖的方式诱导H292细胞中LC3-II的累积。免疫荧光检测发现,白藜芦醇可诱导细胞核和线粒体中GFP-LC3显著增加。(4)自噬抑制剂3-MA能有效减弱白藜芦醇对H292细胞活力的抑制作用,溶酶体酸化抑制剂Bafilomycin A1则可促进白藜芦醇导致的LC3-II累积。(5)白藜芦醇可下调H292细胞中p-Akt、p-P70S6K、p-mTOR蛋白的表达(P<0.05),而对Akt、P70S6K、mTOR蛋白的表达无明显影响(P>0.05)。结论 白藜芦醇可通过抑制Akt/mTOR信号通路抑制肺癌细胞的增殖。 相似文献
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目的 研究香叶木苷对人肝癌HepG2细胞增殖抑制及诱导凋亡的作用,并探讨其相关分子机制。方法 将HepG2细胞分为对照组和香叶木苷组,香叶木苷组分别加入终质量浓度为1、5、25 μg/mL的香叶木苷DMSO溶液,对照组加入等体积的DMSO。药物处理24 h后,台盼蓝染色及Live/Dead染色检测香叶木苷对HepG2细胞活性的影响;CCK-8及EdU染色检测香叶木苷对HepG2细胞增殖的影响;TUNEL染色检测香叶木苷对HepG2细胞凋亡的影响;实时荧光定量PCR(qRTPCR)及Western blotting法检测香叶木苷对Bcl-2、Bax mRNA和蛋白水平的影响。结果 与对照组比较,香叶木苷降低HepG2细胞活力、抑制细胞增殖,5、25 μg/mL组差异显著(P<0.05、0.01、0.001);促进HepG2细胞凋亡,各浓度组均差异显著(P<0.01、0.001),且均呈剂量相关性。经5 μg/mL香叶木苷处理后,HepG2细胞中抗凋亡蛋白Bcl-2的mRNA水平显著降低(P<0.001),而促凋亡蛋白Bax的mRNA水平显著升高(P<0.001),Bcl-2/Bax蛋白水平显著降低(P<0.001)。结论 香叶木苷抑制HepG2细胞活力和增殖、促进凋亡,作用机制与调控Bcl-2/Bax表达有关。 相似文献
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目的 通过构建体外胎盘屏障模型,研究人脐带间充质干细胞(hUC-MSC)对传统胎盘屏障模型功能的影响及其可能的分子机制。方法 将hUC-MSC、人脐静脉内皮细胞(HUVEC)和人滋养层细胞(HTR-8)共同培养于transwell中建立体外胎盘屏障模型,设置对照组(HUVEC+HTR-8)、forskolin组(HUVEC+HTR-8+forskolin)、MSC组(HUVEC+HTR-8+hUC-MSC)、MSC+forskolin组(HUVEC+HTR-8+hUC-MSC+forskolin),通过测量跨膜电阻值、荧光黄CH的渗透性以及P-糖蛋白(P-gp)的活性,评估各组体外胎盘屏障模型的功能;利用实时荧光定量PCR (qRT-PCR)和Westernblotting检测各组体外胎盘屏障模型中P-gp、紧密连接蛋白5(Claudin-5)、闭合小环蛋白-1(ZO-1)、ZO-2、血小板-内皮细胞黏附分子(CD31)的mRNA及蛋白表达水平;利用LC-MS/MS检测阿替洛尔、米诺地尔、美托洛尔3种渗透性工具药透过各组体外胎盘屏障模型的表观渗透系数(Papp),验证模型的功能完整性。结果 与对照组相比,forskolin、MSC、MSC+forskolin组的跨膜电阻值均显著增高(P<0.05、0.001)、P-gp外排功能均增强、荧光黄的Papp值均显著降低(P<0.05、0.01、0.001),且二者联用后作用效果尤为显著,表明该模型具备完整的屏障功能,且MSC+forskolin屏障功能最好;qRT-PCR和Western blotting结果显示,与对照组相比,forskolin组P-gp、ZO-1、ZO-2、CD31的表达显著增加(P<0.05、0.01、0.001),MSC组P-gp、Claudin5、ZO-1和CD31的表达也显著增加(P<0.05、0.01、0.001);联合应用后,各蛋白的mRNA及蛋白表达水平均更显著增加(P<0.01、0.001),表明hUC-MSC增强传统胎盘屏障功能;与对照组相比,各实验组的Papp值均降低,MSC+forskolin组3个工具药均差异显著,美托洛尔差异最显著。结论 hUC-MSC通过增强传统胎盘屏障模型中紧密连接蛋白和外排蛋白的表达,进一步增强了传统胎盘屏障模型的屏障功能。 相似文献
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目的观察索拉非尼联合多柔比星对人乳腺癌MDA-MB-231细胞和人肺癌A549细胞的抑制作用。方法不同浓度索拉非尼联合多柔比星处理人乳腺癌MDA-MB-231细胞和人肺癌A549细胞。①以CCK-8法检测处理24、48和72 h后MDA-MB-231和A549的抑制率;②以细胞划痕试验观察受试细胞的迁移能力;③以印迹试验检测处理24 h后MDAMB-231细胞内P-ERK和Bcl-2的表达情况。结果索拉非尼联合多柔比星能显著抑制人肺癌A549细胞和人乳腺癌MDAMB-231细胞的体外增殖,且具时间依赖性;人乳腺癌MDA-MB-231细胞经不同浓度索拉非尼联合多柔比星处理24 h,P-ERK和Bcl-2蛋白的表达明显下调并呈剂量依赖性。结论索拉非尼联合多柔比星具有抑制人乳腺癌MDA-MB-231细胞和人肺癌A549细胞的增殖,诱导细胞凋亡的作用。 相似文献
12.
《Expert opinion on pharmacotherapy》2013,14(14):2189-2204
Introduction: Academic research has made a significant advancement in understanding the viral causes of cervical cancer and generating the technology for prevention, both at the primary and secondary levels. Human papillomaviruses (HPVs) have been recognized as the first necessary cause of cervical cancer, the second most common cancer in women worldwide. Areas covered: This paper reviews the epidemiological evidence of the causality of HPV in relation to cervical cancer, other genital tract cancers and some cancers of the oral cavity and oropharynx. The review also covers HPV DNA testing as a screening tool. DNA probes of high-risk HPV types in different formats have been fully validated as primary screening tests, as secondary triage tests and as a prognostic marker following treatment of high grade squamous intraepithelial lesions (HSIL). They consistently showed significant superiority over the conventional Pap smears. Biomarkers of the activation of oncogenes (HPV mRNA, p16 and other) are being tested as screening options to improve in sensitivity and specificity, with promising results. HPV vaccines against the two most common HPV types in cancer have completed their Phase III trials with excellent results in efficacy and safety. Combined strategies of HPV vaccination and HPV-based screening tests could theoretically control cervical cancer in any population in which a large coverage with both preventive options is ensured. Accessibility of developing countries to vaccination and low-cost HPV screening options are the barriers to overcome at present. Expert opinion: This paper provides a synthesis of the evidence available supporting the novel paradigm for cervical cancer prevention that has reached a large consensus within the mainstream HPV and cervical cancer prevention research communities. The available technology for prevention and its developments allows real opportunities for cervical cancer elimination in defined populations to be foreseen. 相似文献
13.
胰岛素对人乳腺癌细胞株MDA-MB-543生长的增殖作用 总被引:1,自引:0,他引:1
目的探讨胰岛素对人乳腺癌细胞株MDA-MB-543生长的增殖作用。方法将胰岛素直接作用于体外培养的人乳腺癌细胞株(MDA-MB-543),采用四甲基偶氮唑盐(MTT)法检测细胞增殖,流式细胞仪测定细胞周期分布。结果胰岛素在1~10 mU/mL浓度范围内和作用时间2~16 h范围内,对MDA-MB-543增殖作用逐步增强,反映增殖活性的S期和G2/M期细胞比例逐渐增多,其中S期细胞比例与对照组比较有显著性差异(均P<0.05或0.01)。结论胰岛素能加快诱导MDA-MB-543细胞进入细胞周期S期增殖,呈剂量和时间依赖关系,但是短暂和可逆的。 相似文献
14.
Human breast cancer resistance protein (BCRP/ABCG2) is an ABC-transporter that is present on the luminal membrane of intestinal epithelial cells and restricts absorption of anticancer drugs such as methotrexate, topotecan, mitoxantrone, and doxorubicin. The exact anatomic distribution of BCRP along the gastrointestinal (GI) tract, however, has not been determined before. The aim of this study was, therefore to investigate BCRP mRNA expression pattern along the GI tract in 14 healthy subjects. Furthermore, BCRP duodenal mRNA expression was compared with MDR1/ABCB1 mRNA. Additionally, BCRP mRNA expression was investigated in two human intestinal cell lines (Caco-2 and LS180). Since previous animal studies have suggested sex specific differences in BCRP expression, we analyzed intestinal BCRP expression with respect to sex. Biopsies were taken from different gut segments (duodenum, terminal ileum and ascending, transverse, descending and sigmoid colon). Gene expression was assessed by quantitative real-time PCR (Taqman). BCRP mRNA expression was maximal in the duodenum and decreased continuously down to the rectum (terminal ileum 93.7%, ascending colon 75.8%, transverse colon 66.6%, descending colon 62.8%, and sigmoid colon 50.1% compared to duodenum, respectively). BCRP expression in the duodenum was comparable to MDR1/ABCB1 gene expression. Caco-2 cells showed a comparable expression of BCRP as human duodenal tissue. Gender specific differences in BCRP expression were not observed. These findings represent the first systematic site-specific analysis of BCRP expression along the GI tract. This information might be helpful to develop target strategies for orally administered anticancer drugs. 相似文献
15.
《Expert opinion on drug discovery》2013,8(8):959-968
Introduction: The treatment of penile cancer has changed over the past decade in that it was primarily a surgically managed disease and those with locally advanced or metastatic disease uniformly had a very poor prognosis. However, with the use of better traditional systemic chemotherapeutic agents in the neoadjuvant and adjuvant settings, the disease-specific survival and general outlook has improved. However, there is still a large group of patients who will progress even while on systemic therapy. It is in those patients where the application of targeted therapies has been investigated with some experiencing partial or even complete responses. With the improvement seen in patients with chemotherapy refractory disease, the application of novel targeted agents in the neoadjuvant setting may have a resultant positive impact on patient survival.Areas covered: This review includes research pertaining to targeted therapies, biomarkers and signaling pathways involved with penile cancer. The article was based on a literature search using the keywords ‘penile cancer’ and ‘targeted therapies’.Expert opinion: Penile cancer at the advanced stages of the disease has a high mortality. The utilization of novel targeted therapies in these situations is warranted in combination with, or sequentially with, traditional cytotoxic chemotherapy to improve the patient survival rate. Personalized therapy is nearly here for penile cancer and should be made real within the next decade. 相似文献
16.
《Expert opinion on pharmacotherapy》2013,14(12):2435-2440
In recent years, many new recombinant protein therapeutics have been developed and tested in clinical trials [1]. Current and future clinical uses of recombinant human thyroid-stimulating hormone (rhTSH; Thyrogen?, Genzyme) in thyroid diseases are discussed in the review published in this issue of Expert Opinion on Pharmacotherapy [2]. As Thyrogen is a wild-type rhTSH produced in Chinese hamster ovary cells, it has relatively low affinity to the human TSH receptor. Such low affinity and weak intrinsic bioactivity of rhTSH, compared to the bovine or rodent TSH, may help to explain the results of several studies indicating limited clinical efficacy of Thyrogen. TSH analogues with largely increased receptor affinity, potency and efficacy, are expected to provide not only more effective than currently used diagnostic methods, but should also serve as indispensable second-generation thyrotropins for the diagnosis and treatment of thyroid carcinomas with a largely limited number of TSH receptors. 相似文献
17.
维生素C体外抑制宫颈癌H eLa细胞株生长及其机制的研究 总被引:6,自引:0,他引:6
目的探讨维生素C对人宫颈癌HeLa细胞生长和凋亡的影响,并初步探讨其机制。方法用MTT比色法检测细胞生长抑制作用,流式细胞术测定各组细胞周期分布和凋亡率,以间接免疫荧光法流式细胞术检测相关蛋白的表达,以TRAP-PCR-ELISA法测定端粒酶活性。结果维生素C能以浓度依赖和时间依赖方式阻滞HeLa细胞于G0/G1期,抑制其生长并诱导凋亡。同时HPV18 E6、Bc l-2蛋白表达下调,wtp53、Bax蛋白表达上调,端粒酶活性降低。结论维生素C可抑制HeLa细胞生长,使其细胞周期阻滞于G0/G1期,并诱导其凋亡;其原因在于病毒癌基因E6表达的降低,以及由此而引起的端粒酶活性的降低和细胞内蛋白表达水平的改变,包括HPV18 E6、Bc l-2蛋白表达的下调,wtp53、Bax蛋白表达的上调。 相似文献
18.
目的通过观察人胃癌MKN1细胞的粘附过程和测定整合素β1cDNA的表达水平,研究硫酸右旋糖苷(dextransulfate,DS)对人胃癌MKN1细胞粘附的抑制作用的机制。方法分别在培养液中加入DS或PBS对MKN1细胞进行培养,用荧光免疫细胞染色法和共聚焦显微镜对固定细胞和活细胞在培养盘上的贴壁过程及形态变化进行观察,用RT-PCR测定整合素β1的cDNA表达。结果MKN1细胞通过变形,形成伪足粘附到培养盘,并与其他细胞接触形成单细胞层。免疫染色可见整合素β1在细胞膜上有强烈的表达,并且形成整合素集落。DS抑制整合素β1的表达并使已经形成的整合素集落区域减少;使MKN1细胞的伪足缩短,表现出维持圆形的倾向。在使用DS培养4h后仍有部分细胞处于游离状态,分别收集游离细胞和贴璧细胞,用RT-PCR测定整合素β1的cDNA表达。实验组贴壁细胞和游离细胞内整合素β1的cDNA的表达水平分别减少到对照组细胞的74%和38%。结论DS对人胃癌细胞MKN1粘附过程的抑制与整合素β1表达的减弱有关。 相似文献
19.
Introduction:
Colorectal cancer is the fourth most common malignant disease. Of newly diagnosed patients, 40% have metastatic disease at diagnosis, and approximately 25% of patients with localized disease at diagnosis will ultimately develop metastatic disease. The benefits of systemic chemotherapy in the treatment of metastatic colorectal cancer over best supportive care have been established. Panitumumab (ABX-EGF) is the first fully human monoclonal antibody developed for use in colorectal cancer that targets the extracellular domains of epidermal growth factor receptor.Aims:
The goal of this article is to review the published evidence for the use of panitumumab in the treatment of metastatic colorectal cancer to define its therapeutic potential.Evidence review:
The major evidence of panitumumab activity in colorectal cancer has appeared in meeting report abstracts. One phase II study in monotherapy, one in combination with chemotherapy, and one phase III study have included only patients with metastatic colorectal cancer.Clinical potential:
To date, in phase II clinical studies panitumumab has demonstrated antitumor activity in advanced, refractory colorectal cancer. As monotherapy it resulted in a 10% response rate with 38% of patients having stable disease, and a 36% response rate with 46% stable disease when combined with chemotherapy. A phase III study indicates a clinically significant advantage of panitumumab as third-line monotherapy over best supportive care. Panitumumab appears to have a good tolerability profile, with no maximum tolerated dose yet defined. 相似文献20.
高危型人乳头瘤病毒(human papillomavirus, HPV)感染与宫颈癌的发生、发展关系密切。HPV疫苗在HPV感染所致宫颈疾病防治中的作用逐渐受到重视。本文介绍宫颈癌防治用预防性和治疗性HPV疫苗的研究进展。预防性HPV疫苗中的四价HPV(HPV6/11/16/18)疫苗Gardasil、二价HPV(HPV16/18)疫苗Cervarix和九价HPV (HPV6/11/16/18/31/33/45/52/58)疫苗Gardasil 9已获准上市并用于临床。治疗性HPV疫苗均尚处于研究阶段,且免疫原性与安全性仍有待提高。 相似文献