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miR-200c抑制人乳腺癌MCF-7细胞糖代谢
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作者 陈华波 张崇 +2 位作者 殷焦 肖娟 杨林 《基因组学与应用生物学》 CAS CSCD 北大核心 2019年第6期2874-2878,共5页
为探讨miR-200c对人乳腺癌MCF-7 (Michigan cancer foundation-7)细胞糖代谢水平的影响,本研究使用miR-200c mimics转染MCF-7细胞,通过定量即时聚合酶链锁反应(quantitative real time polymerase chain reaction, qRT-PCR)检测各组细胞... 为探讨miR-200c对人乳腺癌MCF-7 (Michigan cancer foundation-7)细胞糖代谢水平的影响,本研究使用miR-200c mimics转染MCF-7细胞,通过定量即时聚合酶链锁反应(quantitative real time polymerase chain reaction, qRT-PCR)检测各组细胞miR-200c的表达水平;利用细胞计数盒(cell counting kit-8, CCK-8)检测miR-200c mimics转染对MCF-7细胞增殖的影响;通过葡萄糖试剂盒检测各组细胞葡萄糖的消耗,乳酸试剂盒检测各组细胞乳酸的释放量;通过蛋白质印迹法(Western blotting)检测各组细胞糖代谢相关酶己糖激酶(hexokinase 2, HK2)以及肌肉丙酮酸激酶同工酶2 (pyruvate kinase isozyme type M2, PKM2)蛋白表达水平。与miR-NC组相比,miR-200c mimics转染明显上调MCF-7细胞miR-200c m RNA水平;且miR-NC组和MCF-7组miR-200c mRNA水平没有明显差异;细胞计数盒(cell counting kit-8, CCK-8)检测结果显示,与miR-NC组和MCF-7组相比,miR-200c mimics转染不仅明显降低乳腺癌MCF-7细胞的细胞活力,而且显著减少乳腺癌MCF-7细胞葡萄糖的消耗;此外,Western blotting结果显示,miR-200c显著下调MCF-7细胞糖代谢相关酶HK2和PKM2的表达。综上结果表明,miR-200c会抑制人乳腺癌MCF-7细胞糖代谢。本研究成果为乳腺癌防治提供一定的参考价值。 展开更多
关键词 MIR-200C 乳腺癌 MCF-7 糖代谢
The Evaluation of the Effects of Temozolomide on MGMT Gene Expression in MCF-7 and SKBR3 Human Breast Cancer Cell Lines 预览
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作者 Onur Ero?lu Bü?ra Sevim 《癌症治疗(英文)》 2019年第3期215-228,共14页
Background and Aim: In this study, it was aimed to examine the cytotoxic effect of temozolomide (TMZ) treatment, on MCF-7 and SKBR3 cell lines, to study the methylation levels of MGMT gene expression and gene promoter... Background and Aim: In this study, it was aimed to examine the cytotoxic effect of temozolomide (TMZ) treatment, on MCF-7 and SKBR3 cell lines, to study the methylation levels of MGMT gene expression and gene promoter region. Methods: The MTT test was performed to determine the effective dose of TMZ. The time-dependent cell survival test was performed after the IC50 value was found. Western blotting was performed to determine MGMT gene expression levels. High Resolution Melting (HRM) technique was used to determine the methylation levels of MGMT gene promoter region. Results: TMZ has been shown to have a high cytotoxic effect on SKBR3 cell line and low cytotoxicity on MCF-7. When MGMT expression levels before and after TMZ treatment were observed by western blotting, the gene expression levels of TMZ treatment were shown to decrease in both cell lines. It was observed that MGMT gene promoter region was hypermethylated in two cell lines, and that the application of TMZ further increased the methylation levels in the promoter region. Conclusions: It was seen that TMZ could be used as a single agent in SKBR-3 cell line. With this study on breast cancer, it is expected that temozolomide treatment will lead future in vitro and in vivo studies for breast cancer. 展开更多
关键词 BREAST Cancer TEMOZOLOMIDE MGMT MCF-7 SKBR3 HRM
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p,p′-DDT对乳腺癌细胞MCF-7黏附能力及黏附分子的影响 预览
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作者 陈建欧 王莹琼 +1 位作者 李丽燕 郑旭旭 《浙江医学》 CAS 2019年第9期899-902,共4页
目的 探讨有机氯残留物有效成分p,p′-DDT对乳腺癌细胞MCF-7黏附能力及黏附分子的影响。方法 将10-7mol/L的p,p′-DDT作用于MCF-7 48h后,分别采用细胞聚集试验和结晶紫染色法分析其对MCF-7细胞间黏附率和细胞与基质间黏附率的影响,并采... 目的 探讨有机氯残留物有效成分p,p′-DDT对乳腺癌细胞MCF-7黏附能力及黏附分子的影响。方法 将10-7mol/L的p,p′-DDT作用于MCF-7 48h后,分别采用细胞聚集试验和结晶紫染色法分析其对MCF-7细胞间黏附率和细胞与基质间黏附率的影响,并采用RT-qPCR法和Western blot法检测MCF-7中钙黏附蛋白E(E-cadherin)和CD29 mRNA和蛋白表达水平。结果 10-7mol/L的p,p′-DDT作用MCF-7 48h后,MCF-7细胞间黏附率明显降低,细胞与基质间黏附率明显升高;同时下调了E-cadherin mRNA和蛋白表达水平,上调了CD29 mRNA和蛋白表达水平。结论 p,p′-DDT具有降低MCF-7细胞间黏附并提高细胞与基质黏附的作用。p,p′-DDT可能通过改变黏附关键因子E-cadherin和CD29的表达来影响细胞黏附,进而促进肿瘤细胞的侵袭、转移。 展开更多
关键词 p p′-DDT MCF-7 细胞间黏附 细胞与基质间黏附
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ERK抑制剂U0126通过下调cyclin D1与survivin蛋白表达抑制乳腺癌细胞增殖 预览
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作者 田继华 常思佳 +2 位作者 郭海秀 冀贺 王艳红 《中国药理学通报》 CAS CSCD 北大核心 2019年第8期1061-1066,共6页
目的 研究ERK通路抑制剂U0126对乳腺癌细胞增殖的抑制作用,并探讨其调控机制。方法培养人乳腺癌细胞株MCF-7、MDA-MB231,将细胞分组干预,MTT法检测各组细胞增殖情况;流式细胞仪检测各组细胞周期及细胞凋亡;Western blot检测细胞中p-ERK/... 目的 研究ERK通路抑制剂U0126对乳腺癌细胞增殖的抑制作用,并探讨其调控机制。方法培养人乳腺癌细胞株MCF-7、MDA-MB231,将细胞分组干预,MTT法检测各组细胞增殖情况;流式细胞仪检测各组细胞周期及细胞凋亡;Western blot检测细胞中p-ERK/ERK、cyclin D1、survivin及cleaved caspase-3蛋白表达。结果 MTT结果显示,U0126干预24、48 h后,MCF-7、MDA-MB231细胞抑制率明显增加(P<0.01);MCF-7、MDA-MB231细胞经U0126干预24 h后,检测细胞周期及细胞凋亡,G 0/G 1期细胞比例较对照组明显增加,S及G 2期细胞比例下降(P<0.05);而干预组细胞凋亡率较未干预组明显增多(P<0.01);U0126处理人乳腺癌细胞2 h后,可阻断ERK的磷酸化,减少cyclin D1的蛋白表达,抑制survivin而上调cleaved caspase-3的表达,与对照组相比差异有显著性(P<0.01)。结论 U0126通过阻断MCF-7、MDA-MB231细胞中ERK信号通路,调控cyclin D1,将细胞周期阻断在G 0/G 1期,抑制survivin而增加cleaved caspase-3表达,增加细胞凋亡,继而使乳腺癌细胞MDA-MB231、MCF-7的增殖受到抑制。 展开更多
关键词 ERK U0126 MCF-7 MDA-MB231 CYCLIN D1 SURVIVIN
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SMARCC1对人乳腺癌细胞增殖及端粒酶活性的影响 预览
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作者 柯少波 石薇 +2 位作者 陈佳梅 邱虎 陈永顺 《实用医学杂志》 CAS 北大核心 2019年第15期2375-2378,2383共5页
目的探讨下调SMARCC1对人乳腺癌细胞(MCF-7)增殖及端粒酶活性的影响及其可能的机制。方法采用siRNA下调MCF-7细胞SMARCC1基因,MTT法检测细胞增殖,流式细胞术检测细胞凋亡,ELISA法检测细胞端粒酶活性,分别采用qRT-PCR法及Western Blot检... 目的探讨下调SMARCC1对人乳腺癌细胞(MCF-7)增殖及端粒酶活性的影响及其可能的机制。方法采用siRNA下调MCF-7细胞SMARCC1基因,MTT法检测细胞增殖,流式细胞术检测细胞凋亡,ELISA法检测细胞端粒酶活性,分别采用qRT-PCR法及Western Blot检测细胞凋亡相关Caspase-3、端粒酶相关基因hTERT的m RNA及蛋白表达水平。结果转染后24、48、72和96 h,SMARCC1下调组的MCF-7细胞增殖均低于对照组(P <0.05),且具有时间依赖性;SMARCC1下调组晚期凋亡率(6.8±0.5)%高于对照组晚期凋亡率(0.9±0.1)%;转染24及48 h后检测两组细胞端粒酶活性,结果显示,转染24及48 h后SMARCC1下调组MCF-7细胞端粒酶活性均低于对照组;SMARCC1下调组(0.804±0.014)的MCF-7细胞Caspase-3 m RNA表达水平高于于对照组[(0.478±0.005),(t=5.781,P <0.01)];SMARCC1下调组(0.395±0.010)的MCF-7细胞hTERT mRNA表达水平低于对照组[(0.739±0.008),(t=6.203,P <0.01)]。Western Blot实验结果表明,SMARCC1下调组的MCF-7细胞Caspase-3蛋白表达水平高于对照组(P <0.01);SMARCC1下调组MCF-7细胞的hTERT蛋白表达水平低于对照组(P <0.01)。结论下调SMARCC1抑制了人乳腺癌细胞(MCF-7)细胞增殖及促进其凋亡,其机制可能与端粒酶活性被抑制有关。 展开更多
关键词 乳腺癌 SMARCC1 MCF-7 细胞增殖 细胞凋亡 端粒酶
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Investigation of Methylation Profiles of TP53, Caspase 9, Caspase 8, Caspase 3 Genes Treated with DNA Methyl Transferase Inhibitor (DNMTi) Zebularine (ZEB) and Caffeic Acid Phenethyl Ester (CAPE) on MCF-7 and MDA-MB-231 Breast Cancer Cell Lines 预览
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作者 Onur Eroglu Esin Guvenir Celik +3 位作者 Hacer Kaya Merve Celen Mustafa Karabicici Elif Karacoban 《癌症治疗(英文)》 2019年第1期69-85,共17页
Purpose: MCF-7 (ER+, WTP53) and MDA-MB-231 (ER Met, Mutant P53) Caffeic Acid Phenethyl Ester (CAPE) and DNA Methyl Transferase Inhibitor (DNMTi) in breast cancer cell lines of Zebularine (ZEB) single and combined appl... Purpose: MCF-7 (ER+, WTP53) and MDA-MB-231 (ER Met, Mutant P53) Caffeic Acid Phenethyl Ester (CAPE) and DNA Methyl Transferase Inhibitor (DNMTi) in breast cancer cell lines of Zebularine (ZEB) single and combined application of TP53, caspase-9, caspase 8 and caspase-3 genes as a result of the use of single and combined drug methylation profiles are aimed to be evaluated by specific PCR method. Material-Metods: In the MCF-7 and MDA-MB-231 breast cancer cell lines, MTT test and survival analysis were performed as a result of single and combined application of CAPE and Zebularine and Methylation Specific PCR was performed to examine the methylation of caspase-3, caspase-8, caspase-9 and TP53 genes. Results: According to the results of 24-hour drug administration, the IC50 for the MCF-7 cell line was determined as 200 μM, for CAPE 40 μM and for the combined values of 50 μM ZEB + 5 μM CAPE. The effects of caspase-3, caspase-8, caspase-9 and TP53 genes on the methylation level of ZEB, CAPE and ZEB + CAPE drug combination were determined by using bisulfite modified DNAs in MCF-7 and MDA-MB-231 cell lines. Discussion: In the MCF-7 cell line, the 120 μM ZEB viability rate was 51%, and the viability of 80 μM ZEB MDA-MB-231 breast cancer cells decreased by 59.7%. After 20 μM CAPE, viability in MCF-7 cells decreased by 31% in 120 μM CAPE and MDA-MB-231 cells decreased by 41%. The viability with 40 μM CAPE decreased by 19% in MDA-MB-231 cells. It was found that 20 μM CAPE concentration was associated with TP53 methylation in MCF-7 cell lines. The 80 μM ZEB concentration was found to be closely related to the unmethylated status of the TP53 gene. These results obtained with 50 μM ZEB + 5 μM CAPE application were found to be related to the methylated-unmetylated status of the TP53 gene in half (50%). For the caspase-9 gene of MDA-MB-231 cells, 80 μM ZEB concentration was found to be associated with unmetylated status. The effective use of drugs with low concentrations of the drug dose provides a more appropriate a 展开更多
关键词 MCF-7 MDA-MB-231 ZEBULARINE CAPE Breast Cancer METHYLATION
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胡黄连苷Ⅱ对MCF-7乳腺癌细胞自噬的影响及其作用机制研究 预览
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作者 杨红 周杰 阳晓晴 《中国临床药理学与治疗学》 CAS CSCD 2019年第5期535-540,共6页
目的:探讨胡黄连苷Ⅱ对MCF-7乳腺癌细胞自噬及PI3K/AKT/mTOR通路的影响。方法:50只裸鼠随机分为5组,每组10只,分为模型组、3-MA组、胡黄连苷Ⅱ高剂量(100 mg/kg)、中剂量(10 mg/kg)、低剂量(1 mg/kg)组。体外培养人乳腺癌细胞MCF-7,随... 目的:探讨胡黄连苷Ⅱ对MCF-7乳腺癌细胞自噬及PI3K/AKT/mTOR通路的影响。方法:50只裸鼠随机分为5组,每组10只,分为模型组、3-MA组、胡黄连苷Ⅱ高剂量(100 mg/kg)、中剂量(10 mg/kg)、低剂量(1 mg/kg)组。体外培养人乳腺癌细胞MCF-7,随后移植于裸鼠体内,建立MCF-7乳腺癌皮下移植瘤模型。测量各组裸鼠体质量;测量乳腺肿瘤体积并计算出肿瘤抑制率;HE染色法观察肿瘤细胞形态;TUNEL法检测MCF-7细胞凋亡情况;Western blot检测Beclin1、PI3K、p-PI3K、AKT、p-AKT、mTOR、p-mTOR蛋白的表达。结果:胡黄连苷Ⅱ能显著抑制乳腺癌裸鼠体质量的降低(P<0.01);提高肿瘤抑制率(P<0.01);改善病理组织结果;促进MCF-7细胞凋亡;增加Beclin1蛋白的表达;降低PI3K、p-PI3K、AKT、p-AKT、mTOR、p-mTOR蛋白的表达(P<0.01)。结论:胡黄连苷Ⅱ对MCF-7乳腺癌细胞具有显著抑制作用,其机制与抑制PI3K/AKT/mTOR通路从而增强MCF-7细胞自噬有关。 展开更多
关键词 胡黄连苷 MCF-7 自噬 PI3K/AKT/MTOR
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全蝎白术白头翁组合发酵品不同醇浓度提取物的活性成分分析及体外药理研究 预览
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作者 刘金虎 赵翠燕 +8 位作者 孙志艺 王宇 陈宏飞 方园 毛会秀 张瑞 张欣欣 王集会 史磊 《当代化工》 CAS 2019年第6期1170-1173,共4页
评价全蝎白术白头翁组合发酵品(SAPZFP)不同醇浓度提取物的活性成分含量及体外抗肿瘤活性差异。分别测定SAPZFP不同醇浓度提取物的醇溶性总蛋白、总多糖、总黄酮的含量,并采用MTT法检测不同醇浓度提取物抑制肿瘤细胞体外增殖的能力。SAP... 评价全蝎白术白头翁组合发酵品(SAPZFP)不同醇浓度提取物的活性成分含量及体外抗肿瘤活性差异。分别测定SAPZFP不同醇浓度提取物的醇溶性总蛋白、总多糖、总黄酮的含量,并采用MTT法检测不同醇浓度提取物抑制肿瘤细胞体外增殖的能力。SAPZFP不同醇浓度提取物均具有体外抗肿瘤活性,其中75%醇提物抑制乳腺癌细胞株MCF-7、肺腺癌细胞株A549体外增殖的能力最强,IC50分别为0.066、0.022 mg·mL-1。综上所述,SAPZFP的25%、50%、75%醇提物均具有体外抗肿瘤活性,且75%醇提物效果最优。 展开更多
关键词 SAPZFP 双向固体发酵 醇溶性活性成分 A549 MCF-7 抗肿瘤
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沉默RRM1可逆转乳腺癌细胞MCF-7/R对紫杉醇的耐药性 预览
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作者 田楠楠 周磊 +4 位作者 杨丹妮 吴焕贤 马韵词 吕琳 吴少瑜 《南方医科大学学报》 CAS CSCD 北大核心 2019年第3期304-312,共9页
目的阐明沉默核苷酸还原酶M1亚基(RRM1)对乳腺癌耐药细胞MCF-7/R逆转耐药的作用。方法通过高浓度紫杉醇诱导耐药株MCF-7/R;运用Kaplan-Meier Plotter绘制RRM1基因的生存曲线;通过siRNA沉默MCF-7/R细胞中RRM1基因表达,并用Western blot和... 目的阐明沉默核苷酸还原酶M1亚基(RRM1)对乳腺癌耐药细胞MCF-7/R逆转耐药的作用。方法通过高浓度紫杉醇诱导耐药株MCF-7/R;运用Kaplan-Meier Plotter绘制RRM1基因的生存曲线;通过siRNA沉默MCF-7/R细胞中RRM1基因表达,并用Western blot和qRT-PCR方法检测蛋白和基因水平的表达,筛选出高效特异的si-RRM1序列;将该si-RRM1序列转染MCF-7/R细胞,筛选得到能稳定抑制RRM1基因表达的细胞株MCF-7/R/siRNA;四甲基偶氮唑盐(MTT)法和5-乙炔基-2’脱氧尿嘧啶核苷(EdU)染色法检测RRM1沉默后MCF-7/R细胞增殖能力的变化;流式细胞术检测细胞周期和凋亡,并观察周期、凋亡相关蛋白的变化;构建裸鼠皮下移植瘤模型,观察沉默RRM1后给予紫杉醇治疗对裸鼠体内抑瘤效果的影响。结果生存曲线分析显示RRM1基因表达与乳腺癌患者的生存率呈负相关(P=0.000);MCF-7/R细胞中证实RRM1蛋白和mRNA表达水平较MCF-7细胞均显著升高(P<0.01);si-RRM1序列筛选中,转染si-RRM1-04组细胞的RRM1蛋白和mRNA表达量降低最为显著(P<0.001);沉默RRM1后,MCF-7/R细胞对紫杉醇的敏感性显著增加,细胞晚期凋亡比例明显升高(P<0.001),同时降低Akt蛋白的磷酸化并抑制凋亡蛋白Bcl-2的表达,促进p53蛋白表达水平的增加(P<0.001);裸鼠实验显示,与si-NC组相比,沉默RRM1后给予紫杉醇治疗可显著抑制裸鼠体内肿瘤的生长(P<0.001)。结论沉默RRM1可通过诱导细胞凋亡增加提高MCF-7/R细胞化疗敏感性,逆转乳腺癌紫杉醇化疗耐药。 展开更多
关键词 核苷酸还原酶M1亚基 乳腺癌 SIRNA 紫杉醇 MCF-7 耐药
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丹蒽醌对乳腺癌细胞MCF-7增殖及侵袭转移的抑制作用及其作用机制研究
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作者 吕金锋 裴继花 王晓明 《药物评价研究》 CAS 2019年第10期1950-1954,共5页
目的研究丹蒽醌对乳腺癌细胞MCF-7增殖及侵袭转移的抑制作用,并探讨其作用机制。方法 CCK-8法检测不同浓度(10、20、40、60、80、100μmol/L)的丹蒽醌作用24、48 h对乳腺癌细胞MCF-7增殖能力的影响;Transwell实验考察丹蒽醌对乳腺癌细胞... 目的研究丹蒽醌对乳腺癌细胞MCF-7增殖及侵袭转移的抑制作用,并探讨其作用机制。方法 CCK-8法检测不同浓度(10、20、40、60、80、100μmol/L)的丹蒽醌作用24、48 h对乳腺癌细胞MCF-7增殖能力的影响;Transwell实验考察丹蒽醌对乳腺癌细胞MCF-7侵袭转移能力的影响。实时荧光当量PCR(RT-qPCR)法检测c-Myc、Cyclin D1 mRNA的表达水平;Western blotting法检测p-AMPKα、ACC、c-Myc、Cyclin D1蛋白的表达水平。结果不同浓度的丹蒽醌作用不同时间对乳腺癌细胞MCF-7增殖均具有抑制作用;20、40μmol/L的丹蒽醌能够明显的抑制乳腺癌细胞MCF-7的侵袭转移,同时能够激活p-AMPKα的表达,抑制ACC、c-Myc、Cyclin D1等基因的表达,从而抑制乳腺癌细胞MCF-7增殖。结论丹蒽醌对乳腺癌细胞MCF-7增殖及侵袭转移具有抑制作用,其作用机制可能与激活AMPK信号通路抑制c-Myc、Cyclin D1等增殖相关基因表达有关。 展开更多
关键词 丹蒽醌 乳腺癌 MCF-7 侵袭转移 增殖
Triple Effect of Doxorubicin, 5-Fluorouracil, Propranolol on Cell Survival on MCF-7 Breast Cancer Cell Line 预览
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作者 Onur Eroglu Hacer Kaya +3 位作者 Esin Guvenir Celik Merve Celen Elif Korkut Nagihan Nizam 《生物科学与医学(英文)》 2019年第2期74-85,共12页
Purpose: Investigating the triple effect of doxorubicin, 5-fluorouracil, propranolol on MCF-7 (ER+, WTp53) breast cancer cell line with MTT test and survival analysis. Materials/Methods: In order to determine effectiv... Purpose: Investigating the triple effect of doxorubicin, 5-fluorouracil, propranolol on MCF-7 (ER+, WTp53) breast cancer cell line with MTT test and survival analysis. Materials/Methods: In order to determine effective dosages of a combination of doxorubicin, 5-fluorouracil, propranolol on the MCF-7 cell line by using MTT and survival analysis technique. Result: IC50 values acquired by MTT tests are 0.01 mg/ml for doxorubicin, 6 mg/ml for 5-fluorouracil, 30 mg/ml for propranolol and 0.2/1/30 mg/ml (with previous respect) if all three agents are combined. It is found that the use of doxorubicin, 5-fluorouracil, and propranolol in combination is much effective than their single application. Discussion: Moderate concentrations of doxorubicin, 5-fluorouracil, and propranolol, if they are applied individually, showed high toxicity. When we used these drugs in combination;toxic effects lessened with respect to monotherapy. In the MCF-7 cell line, doxorubicin (IC50: 0.01 μM) increases cell death rates significantly and propranolol (IC50: 3 μM) has minimum effects in monotherapy in contrast to others. Propranolol is only superior to itself in combination therapy (IC50: 4 μM). However 5-fluorouracil (IC50: 30 μM) showed antagonistic effects with respect to other drugs. Additionally, having applied the three drugs in combination on the MCF-7 cell line for the first time in literature, it is highly possible to assess the application of doxorubicin, 5-fluorouracil and propranolol combination as a novel therapy option. 展开更多
关键词 MCF-7 Breast Cancer COMBINE Treatment DOXORUBICIN 5-FLUOROURACIL PROPRANOLOL
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miR-221增强乳腺癌细胞对多西他赛的耐药性 预览
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作者 刘吴瑕 施洪 +2 位作者 陆胜莲 刘超乾 楼国良 《现代肿瘤医学》 CAS 2019年第24期4341-4345,共5页
目的:探究miR-221在人乳腺癌细胞T47D和MCF-7多西他赛(docetaxel)耐药性中的作用及机制。方法:qPCR检测多西他赛处理乳腺癌细胞T47D和MCF-7不同时间点,细胞中miR-221含量的变化;qPCR和Westernblot检测miR-221mimics的转染效率。用阴性对... 目的:探究miR-221在人乳腺癌细胞T47D和MCF-7多西他赛(docetaxel)耐药性中的作用及机制。方法:qPCR检测多西他赛处理乳腺癌细胞T47D和MCF-7不同时间点,细胞中miR-221含量的变化;qPCR和Westernblot检测miR-221mimics的转染效率。用阴性对照(NC)或miR-221mimics转染细胞,不同浓度的多西他赛刺激细胞72小时后,MTT法检测细胞对多西他赛的耐药性;PI和AnnexinV双染法检测miR-221过表达对T47D和MCF-7细胞凋亡的影响;qPCR和Westernblot检测靶蛋白p27的表达。结果:在T47D和MCD-7中多西他赛刺激明显促进miR-221的表达量升高;miR-221在细胞内可以发挥生物学效应,降低靶蛋白p27的表达;且过表达miR-221明显增强T47D和MCF-7对多西他赛的耐药性,降低其凋亡率。结论:miR-221过表达可明显增强T47D和MCF-7细胞对多西他赛的耐药性。 展开更多
关键词 MIR-221 T47D MCF-7 耐药性 多西他赛
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Effect of Marsdenia tenacissima extract on G2/M cell cycle arrest by upregulating 14-3-3σ and downregulating c-myc in vitro and in vivo
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作者 Li Sun Qurat UI Ain +3 位作者 Ying-sheng Gao Ghulam Jilany Khan Sheng-tao Yuan Debmalya Roy 《中草药:英文版》 CAS 2019年第2期169-176,共8页
Objective: Marsdenia tenacissima extract(MTE) is a traditional Chinese herbal medicine with anti-cancer activity. In some previous studies, different mechanism actions of the anti-cancer effect of MTE have been reveal... Objective: Marsdenia tenacissima extract(MTE) is a traditional Chinese herbal medicine with anti-cancer activity. In some previous studies, different mechanism actions of the anti-cancer effect of MTE have been revealed. In this study, we first observed that MTE exhibited G2/M cell cycle arrest on two different human breast cancer cell lines, MDA-MB-231 and MCF-7 by mediating 14-3-3σ and c-myc.Methods: The effect of MTE on G2/M cell cycle arrest was evaluated in MDA-MB-231 and MCF-7 cell lines. MTT assay was done for evaluation of cell viability. Flow cytometry was employed for cell cycle analysis. Western blotting analysis and immunohistochemistry were performed to analyze the expression of G2/M cell cycle-related key protein in cells and tissue samples. Animal studies have been conducted to elucidate the anti-tumor effect of MTE.Results: Cell cycle is the backbone for developing cancer. Cell cycle proteins play a major role in the progression of cell cycle and cell proliferation. However, some key protein directly or indirectly modulate the action of cell cycle protein that highly affect cell cycle regulation. In order to investigate cellular proliferation of cancer, we observed that MTE induced the upregulation of 14-3-3σ and downregulation of c-myc,and then reduced the expression of G2/M cell cycle associated key protein, leading to the inhibition of cellular entry into mitosis phase. We also confirmed that MTE exerted a significant antitumor effect on the MDA-MB-231 xenograft model in vivo.Conclusion: G2/M cell cycle arrest occurred by the action of MTE, mediated by the upregulation of 14-3-3σ as well as downregulation of c-myc in MDA-MB-231 and MCF-7 cell lines. 展开更多
关键词 C-MYC G2/M ARREST Marsdenia tenacissima EXTRACT MCF-7 MDA-MB-231 14-3-3σ
Antiproliferative and apoptosis-inducing potential of 3β-hydroxy-Δ5-steroidal congeners purified from the soft coral Dendronephthya putteri 预览
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作者 Thilina U. JAYAWARDENA Won Woo LEE +6 位作者 I. P. Shanura FERNANDO K. K. Asanka SANJEEWA Lei WANG Tee Gee LEE Young Jin PARK Chang-ik KO You-Jin JEON 《海洋湖沼学报(英文)》 SCIE CAS CSCD 2019年第4期1382-1392,共11页
The exploration and identification of antiproliferative phytochemicals have received increased attention in medicinal chemistry. In particular, research focused on the toxicology of marine natural products has increas... The exploration and identification of antiproliferative phytochemicals have received increased attention in medicinal chemistry. In particular, research focused on the toxicology of marine natural products has increased in recent years. Terpenoids, among many secondary metabolites, have been demonstrated to act as effective anticancer agents. Soft corals, a group of marine invertebrates, produce a variety of terpenoids with biofunctional properties. The current study presents the extraction, purification, and identification of sterol congeners from the soft coral Dendronephthya putteri. The method involves 50% chloroform-methanol extraction, polar column fractionation, and analysis through GC-MSn. Dose-dependent antiproliferative activity was observed within the sterol-rich fraction (DPCMH 2-4), which consisted of 3β-hydroxy-Δ5-steroidal congeners. This fraction inhibited the growth of HL-60 and MCF-7 cells with IC50 values of 25.27±1.43 and 22.81±0.15 μg/mL, respectively. Apoptotic body formation, DNA damage, cell cycle arrest, and apoptotic cell signaling pathway activation were also observed, reinforcing the dose-dependent antiproliferative and apoptosis-inducing activity of 3β-hydroxy-Δ5-steroidal congeners. To our knowledge, this is the first report of anticancer agent identification from the soft coral D. putteri. Based on the observations, these steroidal congeners are promising candidates for the development of anticancer drugs. 展开更多
关键词 Dendronephthya putteri soft CORAL ANTIPROLIFERATIVE agent HL-60 MCF-7 apoptosis steroidal CONGENERS
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Cancer cell detection and imaging: MRI-SERS bimodal splat-shaped Fe3O4/Au nanocomposites
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作者 Xinmei Zhao Leyong Zeng +2 位作者 Narayan Hosmane Yan Gong Aiguo Wu 《中国化学快报:英文版》 SCIE CAS CSCD 2019年第1期87-89,共3页
The development of multifunctional contrast agents contributes significant character in the diagnosis of cancer. However, still efforts are required to design and improve the biocompatibility of contrast agents for ea... The development of multifunctional contrast agents contributes significant character in the diagnosis of cancer. However, still efforts are required to design and improve the biocompatibility of contrast agents for early detection of cancer. Herein, we synthesized splat shape Fe3O4/Au nanocomposites for multimode biomedical applications. Transmission electron microscopy(TEM) results showed that the splat-like Fe3O4/Au structure was in the range of 130 nm and homogeneously distributed in the aqueous medium. The nanocomposites were incubated with MCF-7 cells to investigate the magnetic resonance imaging(MRI) and surface-enhanced Raman scattering(SERS) activities. The excellent T2 MRI and enhanced SERS properties were obtained without any cytotoxicity. These results demonstrated that assynthesized splat-shaped Fe3O4/Au nanocomposites may be a promising MRI/SERS dual probe for the tumor detection. 展开更多
关键词 Fe3O4/Au MRI SERS Cell DETECTION MCF-7
蒙花苷对MCF-7雄激素受体的影响 预览
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作者 左志琴 曾文雪 +2 位作者 丁舸 黄冰林 沈志华 《江西中医药》 2019年第1期62-64,共3页
目的:观察蒙花苷对MCF-7细胞雄激素受体(AR)的影响。方法:培养MCF-7细胞,给予不同浓度(0,2,6.7,20,66.7,200μg/mL)蒙花苷处理后,CCK-8检测细胞活性,real-time PCR检测细胞AR mRNA的表达。结果:与空白组相比,经蒙花苷处理后,MCF-7活性... 目的:观察蒙花苷对MCF-7细胞雄激素受体(AR)的影响。方法:培养MCF-7细胞,给予不同浓度(0,2,6.7,20,66.7,200μg/mL)蒙花苷处理后,CCK-8检测细胞活性,real-time PCR检测细胞AR mRNA的表达。结果:与空白组相比,经蒙花苷处理后,MCF-7活性无明显抑制(P>0.05),AR mRNA呈先升高后降低趋势,其中当蒙花苷浓度为6.7…μg/mL时AR表达量最高,66.7μg/mL时表达量最低。结论:蒙花苷对MCF-7细胞AR表达具有双向调节作用,这种作用与浓度有关。 展开更多
关键词 蒙花苷 MCF-7 雄激素受体
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PRMT2β suppresses autophagy and glycolysis pathway in human breast cancer MCF-7 cell lines
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作者 Yajun Chenx Xianpeng Dai +7 位作者 Yao Yao Jing Wang Xinzhi Yang Yunsheng Zhang Jing Yang Renxian Cao Gebo Wen Jing Zhong 《生物化学与生物物理学报:英文版》 SCIE CAS CSCD 2019年第3期335-337,共3页
Autophagy as a novel therapeutic target can inhibit or increase treatment efficacy in various types of breast cancer in a cell-type-dependent manner [1,2].Several studies have revealed that the coordination between Ak... Autophagy as a novel therapeutic target can inhibit or increase treatment efficacy in various types of breast cancer in a cell-type-dependent manner [1,2].Several studies have revealed that the coordination between Akt and the glycolytic pathway plays an indispensable role in mediating autophagy and caspase-dependent apoptosis,suggesting that a new regulatory mechanism for the process [3,4].Protein arginine N-methyltransferases(PRMTs)are eukaryotic enzymes that catalyze the transfer of methyl groups from S-adenosylmethionine to arginine residues of numerous PRMT substrates [5,6].PRMT2(also known as HRMT1L1)belongs to the arginine methyltransferase family [7].PRMT2β is a novel PRMT2 splice variant isolated from breast cancer cell [8].It occurs at the 3′ end of the PRMT2,resulting in loss of exons 7–9 and downstream frame-shifting [9].PRMT2β possesses 83 new amino acids at the C-terminus and its size is 301 amino acids.Our previous study reported that PRMT2β has potential antitumor effect by suppressing cyclin D1 expression [10].However,little is known about whether PRMT2β could regulate autophagy and glycolysis of MCF-7 cells. 展开更多
关键词 MCF-7 apoptosis expression treatment CYCLIN can Akt its
Sonic Hedgehog stimulates migration of MCF-7 breast cancer cells through Rac1 预览
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作者 Tian Shen Bo'ang Han +4 位作者 Yan Leng Sen Yan Junfeng Shi Shen Yue Steven Y Cheng 《生物医学研究杂志:英文版》 CAS CSCD 2019年第5期297-307,共11页
As one of the most common tumors in women, breast cancer has drawn considerable interest from investigators and clinicians in recent years. Despite early diagnosis and best therapeutic regimens available, the prognosi... As one of the most common tumors in women, breast cancer has drawn considerable interest from investigators and clinicians in recent years. Despite early diagnosis and best therapeutic regimens available, the prognosis of malignant or metastatic breast cancer patients is still not optimistic. Hedgehog signaling, a classical pathway indispensable to embryonic development, participates in the growth of a variety of tumors. In the present study,the effect of Sonic Hedgehog(Shh) on breast cancer cells was investigated. We identified that Shh signal stimulated the migration of MCF-7 breast cancer cells. Smo and Gli1 were involved in Shh-stimulated migration of MCF-7 cells. Activating Smo and Gli1 induced cell migration, which was blocked by their specific antagonists.The effect of Shh signaling on MCF-7 cells was independent of Wnt5 a, Dvl2 and Rab35, but directly dependent on Rac1. In conclusion, our study suggested that Shh promotes breast cancer cell migration via Rac1 independently of the non-canonical Wnt signaling pathway, which may represent a rational molecular target for combination medication in breast cancer. 展开更多
关键词 Sonic HEDGEHOG RAC1 BREAST cancer MCF-7 MIGRATION
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SAHA抑制乳腺癌ER受体阳性细胞系MCF-7细胞侵袭的形态学观察 预览
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作者 刘春阳 周伟强 《沈阳医学院学报》 2018年第2期181-184,共4页
目的:研究SAHA对乳腺癌雌激素受体阳性细胞系MCF-7细胞侵袭力的影响。方法:采用细胞增殖实验、细胞划痕、Transwell细胞侵袭力测定等实验从形态学角度观察SAHA对MCF-7细胞侵袭力的影响。结果:与Leptin处理组相比,SAHA明显抑制了MCF-7细... 目的:研究SAHA对乳腺癌雌激素受体阳性细胞系MCF-7细胞侵袭力的影响。方法:采用细胞增殖实验、细胞划痕、Transwell细胞侵袭力测定等实验从形态学角度观察SAHA对MCF-7细胞侵袭力的影响。结果:与Leptin处理组相比,SAHA明显抑制了MCF-7细胞内DNA复制能力,并限制了其游走性。Transwell实验也证实SAHA处理后的细胞侵袭性较对照组细胞明显减弱,细胞状态较差,呈星状和针刺样。结论:SAHA抑制了乳腺癌MCF-7细胞的侵袭力。 展开更多
关键词 乳腺癌 MCF-7 细胞侵袭力
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β-榄香烯对人乳腺癌细胞侵袭和迁移作用的研究 被引量:1
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作者 郭婷婷 黄炜平 +5 位作者 胡晨霞 杨科 李建国 王剑 张奉学 王洪琦 《中药药理与临床》 CSCD 北大核心 2018年第1期76-80,共5页
目的:研究β-榄香烯对不同分子亚型人乳腺癌细胞增殖、侵袭和迁移的作用。方法:以不同转移潜能MCF-7、MDAMB-231乳腺癌细胞作为研究对象,设空白对照组及药物组,药物组以不同浓度β-榄香烯溶液作用细胞24h与48h后,CCK8法检测其对细胞... 目的:研究β-榄香烯对不同分子亚型人乳腺癌细胞增殖、侵袭和迁移的作用。方法:以不同转移潜能MCF-7、MDAMB-231乳腺癌细胞作为研究对象,设空白对照组及药物组,药物组以不同浓度β-榄香烯溶液作用细胞24h与48h后,CCK8法检测其对细胞活力的影响。应用细胞克隆形成实验进一步检测β-榄香烯对两种细胞增殖和克隆形成能力的影响。此外,Transwell实验和划痕实验检测β-榄香烯对高转移性细胞株MDA-MB-231细胞侵袭和迁移能力的作用。结果:β-榄香烯对MCF-7、MDA-MB-231乳腺癌细胞的活力均有抑制作用,且对高转移细胞MDA-MB-231抑制作用更强,对于MCF-7细胞24h,48h的半数抑制浓度(IC50)分别为(43.45±0.43),(43.05±0.56)μg/ml,对MDA-MB-231细胞24h,48h的半数抑制浓度(IC50)分别为(12.20±0.61),(8.30±0.27)μg/ml。克隆形成实验结果表明β-榄香烯能够抑制乳腺癌细胞的克隆形成率,与空白对照组相比具有显著性差异。当β-榄香烯浓度为25μg/ml时,对MDA-MB-231细胞的抑制率达到49.2%,对MCF-7只有15.5%。此外,Transwell实验和划痕实验结果显示当β-榄香烯浓度达到10μg/ml时就能抑制高转移性细胞株MDA-MB-231的侵袭和迁移能力。结论:β-榄香烯能够抑制MCF-7、MDA-MB-231的细胞活力、增殖和克隆形成,且对高转移性细胞株MDA-MB-231的侵袭和迁移能力显示出很强的抑制作用,其具体作用机制有待进一步研究。 展开更多
关键词 Β-榄香烯 MCF-7 MDA-MB-231 乳腺癌
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