期刊文献+
共找到49篇文章
< 1 2 3 >
每页显示 20 50 100
Potential roles of EZH2, Bmi-1 and mi R-203 in cell proliferation and invasion in hepatocellular carcinoma cell line Hep3B 被引量:12
1
作者 Fang Yang Li-Zhi Lv +1 位作者 Qiu-Cheng Cai Yi Jiang 《World Journal of Gastroenterology》 SCIE CAS 2015年第47期13268-13276,共9页
AIM: To investigate the potential roles of enhancer of zeste homolog2(EZH2), Bmi-1 and mi R-203 in cell proliferation and invasion in hepatocellular carcinoma(HCC) cell line Hep3 B.METHODS: A total of 73 patients who ... AIM: To investigate the potential roles of enhancer of zeste homolog2(EZH2), Bmi-1 and mi R-203 in cell proliferation and invasion in hepatocellular carcinoma(HCC) cell line Hep3 B.METHODS: A total of 73 patients who underwent surgical resection at Fuzong Clinical Medical College of Fujian Medical University were enrolled in this study. Hep3 B cells were cultivated in RPMI 1640 medium supplemented with 10% fetal bovine serum at 37?℃. Vectors that containing c DNA of the EZH2 gene or mi R-203 targeted sh RNA plasmid were constructed, and then transfected into Hep3 B cells. The m RNA expression of mi R-203, EZH2, and Bmi-1 was analyzed using quantitative real-time polymerase chain reaction analysis, and the protein levels of EZH2 and Bmi-1 were detected by Western blot analysis. Effect of EZH2 or mi R-203 on cell proliferation was observed by methyl thiazolyl tetrazolium assay, and cell apoptosis was assessed using flow cytometry. Besides, effect of EZH2 or mi R-203 on tumor cell invasion was detected using Transwell assay.RESULTS: The m RNA levels of EZH2 and Bmi-1 in HCC tissues and in Hep3 B cells were significantly higher compared with those in normal samples(P < 0.01), while mi R-203 level was significantly lower in HCC tissues(P < 0.01). Hep3 B cells transfected with EZH2-sh RNA or mi R-203-sh RNA showed lower expression levels of EZH2 and Bmi-1(P < 0.05). Compared with controls, Hep3 B cells transfected with EZH2-sh RNA had relative slow cell proliferation, indicating that low expression of EZH2 and Bmi-1 and overexpression of mi R-203 could inhibit Hep3 B cell proliferation(P < 0.05). The average apoptosis rate of Hep3 B cells transfected with EZH2-sh RNA vector was about 18.631%, while that of Hep3 B cells transfected with sh RNA vector was about 5.33%, suggesting that EZH2 was down-regulated by transfecting with EZH2-sh RNA, and the down-regulated EZH2 contributed to the cell apoptosis. Low expression of EZH2 and Bmi-1 and overexpression of mi R-203 could reduce Hep3 B cell invasion(P < 0.05).CONCLUSION: Our study suggests that EZH2 and Bmi-1 are up-regulated while mi R-203 is downregulated in Hep3 B cells. Mi R-203 may contribute to the metastasis and enhance apoptosis of HCC cells by regulating EZH2 and Bmi-1. Our study may provide a theoretical basis for metastasis of HCC and targeted therapy of HCC. 展开更多
关键词 EZH2 BMI-1 miR-203 Hepatocellularcarcinoma HEP3B cell line INVASION PROLIFERATION
下载PDF
MiR-25-3p attenuates the proliferation of tongue squamous cell carcinoma cell line Tca8113 被引量:3
2
作者 Jia-Ying Xu Li-Li Yang +3 位作者 Chao Ma Yuan-Liang Huang Gui-Xiang Zhu Qi-Lin Chen 《Asian Pacific Journal of Tropical Medicine》 SCIE CAS 2013年第9期743-747,共5页
Objective:To investigate the effects of miR-25-3p on the occurrence,development and proliferation of tongue squamous cell carcinoma cells.Methods:To establish tongue squamous cell carcinoma cell line Tca8113 that stab... Objective:To investigate the effects of miR-25-3p on the occurrence,development and proliferation of tongue squamous cell carcinoma cells.Methods:To establish tongue squamous cell carcinoma cell line Tca8113 that stably and highly express miR-25-3p using recombinant reiroviral vector-mediated gene transfer method.The proliferation of transfected Tca8113 was detected by thiazolyl blue tetrazolium bromide(MTT)and cell colony formation assays.eyclnD1,p21^(cipt)and p27^(kipt)mRNA expressions in the transfected Tca-8113 were detected by quantitative PCR.cyclinD1,p21^(cipt),p27^(kipt),AKT,p-AKT,FOXOt and p-FOX01 expressions in the transfected Tca8113 were detected by western blot analysis.In addition,miR-25-3p expression in the tongue squamous cell carcinoma cell line and tissue specimen was also detected by quantitative PCR.Results:Quantitative PCR showed that mitt-25-3p expression in the tongue squamous cell carcinoma cell lines and tissue specimen was significantly lower than that in the adjacent tissue.MTT and cell colony formation assays showed that after miR-25-3p overexpression,the proliferation of transfected Tca8113 was obviously attenuated.Western blot analysis and quantitative PCR showed that after miR-25-3p overexpression.p21^(cipt)and p27^(kipt)expressions were upregulated,while cyclinD1,AKT,FOXO1 expressions were downregulated,and AKT and FOXO1 phosphorylation was inactivated in the transfected Tca8113 cells.Conclusions:MiR-25-3p inhibited the proliferation of tongue squamous cell carcinoma cells and regulated cell cycle-related protein expression,playing an important role in the occurrence and development of squamous cell carcinoma of the tongue. 展开更多
关键词 MiR-25-3p Tongue SQUAMOUS cell carcinoma cellular PROLIFERATION RETROVIRUS Stable cell line AKT/FOXO1
下载PDF
Contragestazol (DL111-IT) inhibits proliferation of human androgen-independent prostate cancer cell line PC3 in vitro and in vivo 被引量:2
3
作者 Qiao-Jun He Bo Yang Yi-Jia Lou Rui-Ying Fang 《Asian Journal of Andrology》 SCIE CAS CSCD 2005年第4期389-393, ,共5页
Aim: To evaluate the antiproliferative activity of contragestazol (DL111-IT) on the human prostate cancer cell line PC3 in vitro and in vivo and to elucidate its potential molecular mechanisms. Methods: The cell k... Aim: To evaluate the antiproliferative activity of contragestazol (DL111-IT) on the human prostate cancer cell line PC3 in vitro and in vivo and to elucidate its potential molecular mechanisms. Methods: The cell killing ability of DL111-IT was measured by the 3-(4,5-dimethylthia-zol,2-yl)-2,5-diphenyltetrazolium bromide (MTT) reagent assay method and the tumor xenograft model. The cell cycle was analyzed by flow cytometry and protein expression, including retinoblastoma (pRb), cyclin-dependent kinase 4 (CDK4) and cyclin D 1, was detected by Western blotting. Results: DL111-IT exhibited high efficiency on cell growth inhibition of the human androgen-independent prostate cancer cell line PC3. The drug concentration that yielded 50 % cell inhibition (IC50 value) was 9.9 mg/mL. In the PC3 tumor xenograft study, DL111-IT (1.25 mg/kg-20.0 mg/kg) given once a day for 10 days significantly inhibited tumor growth, with the inhibition rate ranging from 21% to 50 %. Flow cytometric analysis indicated that DL111-IT could cause GI arrest in the PC3 cell line, but not apoptosis. DL111-IT enhanced pRb expression and down-regulated CDK4 and cyclin D 1 expression, suggesting that cell cycle regulation might contribute to the anticancer property of DL 111- IT. Conclusion: DL111-1T inhibits the proliferation of human androgen-independent prostate cancer cell line PC3 in vitro and in vivo by a cell cycle regulation pathway. 展开更多
关键词 DL111-IT prostate cancer PRB cyclin-dependent kinase 4 cyclin D 1 PC3 cell line
下载PDF
氯化锂对KT-1/A3细胞增殖和凋亡的影响
4
作者 唐丽 《激光生物学报》 CAS CSCD 2003年第4期264-268,共5页
目的:研究氯化锂(LiCl)在体外对KT-1/A3白血病细胞增殖及凋亡的影响。方法:采用液体培养实验,MTT实验,集落培养实验为指标观察LiCl对KT-1/A3细胞增殖的影响,采用DNA片段凝胶电泳及流式细胞检测为指标检测细胞凋亡。结果:1不同浓度的LiCl... 目的:研究氯化锂(LiCl)在体外对KT-1/A3白血病细胞增殖及凋亡的影响。方法:采用液体培养实验,MTT实验,集落培养实验为指标观察LiCl对KT-1/A3细胞增殖的影响,采用DNA片段凝胶电泳及流式细胞检测为指标检测细胞凋亡。结果:1不同浓度的LiCl(5mM-25mM)对KT-1/A3细胞具有抑制增殖的作用,这种增殖抑制作用呈剂量依赖关系。2在LiCl(20mM)作用72h的DNA凝胶电泳谱可见DNALadder及流式细胞仪检测可见凋亡特有的AP峰,提示LiCl可诱导KT-1/A3细胞凋亡。结论:LiCl能抑制KT-1/A3白血病细胞增殖和诱导凋亡。 展开更多
关键词 氯化锂(LiCl) 白血病 KT—1/a3细胞株 细胞培养 增殖 凋亡
下载PDF
F1t3 RECEPTOR EXPRESSION ON THE SURFACE OF MALIGNANT HEMATOPOIETIC CELLS AND RESPONSES TO F1t3 LIGAND STIMULATION
5
作者 许志祥 徐颖 +3 位作者 朱剑昆 李彩霞 李颖 张学光 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 2000年第4期263-267,共5页
Objective: To investigate the F1t3 receptor expression on the surface of malignant hematopoietic cells, the effect of TNFα and dexamethasone (DXM) on its expression and the responses of those cells to recombinant hum... Objective: To investigate the F1t3 receptor expression on the surface of malignant hematopoietic cells, the effect of TNFα and dexamethasone (DXM) on its expression and the responses of those cells to recombinant human F1t3 ligand (rhFL). Methods: Eighteen malignant hematopoietic cell lines were determined for the F1t3 receptor expression by flow cytometric analysis. The effect of rhFL on the proliferation of malignant hematopoietic cellsin vitro was measured using MTT assay. Results: The expressions of F1t3 receptor on the surface of Raji, Daudi, HL-60, 8266 and XG-6 cells were detected by flow cytometric analysis. Following incubation with 20 ng/ml TNFα for 24h, the number of F1t3 receptor positive cells decreased in Raji and 8266, increased in HL-60 and XG-6, and no difference in Daudi cells. After incubation with 10?6 mol/L DXM for 24h, the number of F1t3 receptor positive cells decreased in all the 5 F1t3 receptor positive cell lines. rhFL stimulated the proliferation of HL-60 and Raji cells. Conclusion: For most of the malignant hematopoietic cells, there was neither the expression of F1t3 receptor nor the response to rhFL. DXM may be useful to reduce the effect of FL on the proliferation of some F1t3 receptor positive malignant hematopoietic cells in vitro andin vivo. 展开更多
关键词 F1t3 receptor Recombinant human F1t3 ligand (rhFL) Malignant hematopoietic cell lines Proliferation Dexamethasone (DXM)
下载PDF
Comparative Analysis of Protein Expression Concomitant with DNA Methyltransferase 3A Depletion in a Melanoma Cell Line
6
作者 Xiaoyan Liu Shengnan Tang +5 位作者 Tonghua Li Haoyue Wang Jiangming Sun Qian Qiao Jun Yao Jian Fei 《American Journal of Analytical Chemistry》 2011年第5期539-572,共34页
DNA methyltransferase 3A (Dnmt3a), a de novo methyltransferase, has attracted a great deal of attention for its important role played in tumorigenesis. We have previously demonstrated that melanoma is unable to grow i... DNA methyltransferase 3A (Dnmt3a), a de novo methyltransferase, has attracted a great deal of attention for its important role played in tumorigenesis. We have previously demonstrated that melanoma is unable to grow in-vivo in conditions of Dnmt3a depletion in a mouse model. In this study, we cultured the Dnmt3a depletion B16 melanoma (Dnmt3a-D) cell line to conduct a comparative analysis of protein expression con-comitant with Dnmt3a depletion in a melanoma cell line. After two-dimensional separation, by gel electro-phoresis and liquid chromatography, combined with mass spectrometry analysis (1DE-LC-MS/MS), the re-sults demonstrated that 467 proteins were up-regulated and 535 proteins were down-regulated in the Dnmt3a-D cell line compared to the negative control (NC) cell line. The Genome Ontology (GO) and KEGG pathway were used to further analyze the altered proteins. KEGG pathway analysis indicated that the MAPK signaling pathway exhibited a greater alteration in proteins, an interesting finding due to the close relation-ship with tumorigenesis. The results strongly suggested that Dnmt3a potentially controls the process of tu-morigenesis through the regulation of the proteins (JNK1, p38α, ERK1, ERK2, and BRAF) involved in tu-mor-related pathways, such as the MAPK signaling pathway and melanoma pathway. 展开更多
关键词 Dnmt3a MELANOMA cell line 1DE-LC-MS/MS MAPK Signaling PATHWAY MELANOMA PATHWAY
下载PDF
表皮生长因子对PC-3细胞内皮素-1及其受体mRNA表达的影响 被引量:4
7
作者 贾瑞鹏 姜彦飞 +4 位作者 许露伟 王书奎 王自正 李文成 何帮顺 《中华男科学杂志》 CAS CSCD 2008年第1期15-19,共5页
目的:探讨表皮生长因子(EGF)对激素非依赖性前列腺癌(HRPC)PC-3细胞中内皮素1(ET-1)及其受体mRNA表达的影响。方法:EGF作用不同时间(0、8、16、24、32、48h)后,RT-PCR法测定PC-3细胞中ET-1及其受体ETAR mRNA、ETBR mRNA表达;EGF干预24h... 目的:探讨表皮生长因子(EGF)对激素非依赖性前列腺癌(HRPC)PC-3细胞中内皮素1(ET-1)及其受体mRNA表达的影响。方法:EGF作用不同时间(0、8、16、24、32、48h)后,RT-PCR法测定PC-3细胞中ET-1及其受体ETAR mRNA、ETBR mRNA表达;EGF干预24h后,RT-PCR法测定ET-1及其受体ETAR mRNA、ETBR mRNA表达变化。结果:在PC-3细胞中可检测到ET-1及ETAR mRNA表达,但无ETBR mRNA表达;EGF可上调ET-1及ETAR mRNA表达,与对照组比较,差异具有显著性;ET-1及ETAR mRNA表达随EGF干预时间增加而增加,EGF作用不同时间对PC-3细胞ET-1、ETAR mRNA表达的影响不同,差异具有显著性(P<0.05)。结论:EGF可上调PC-3细胞中ET-1及ETAR mRNA表达,为HRPC的治疗提供了分子生物学基础。 展开更多
关键词 激素非依赖性前列腺癌 内皮素1 内皮素受体 表皮生长因子 PC-3细胞
下载PDF
猪乙脑病毒分离株BSF.ZZ-1和BSF.ZZ-3在BHK-21细胞上的传代培养及E基因序列稳定性分析 被引量:3
8
作者 胡博 滕蔓 +5 位作者 禹乐乐 罗俊 迟佳琪 宿靖伟 柴书军 张改平 《华北农学报》 CSCD 北大核心 2013年第6期71-76,共6页
为研究猪乙脑病毒(JEV)分离株遗传基因的稳定性,将JEV分离株BSF.ZZ-1和BSF.ZZ-3在BHK-21细胞上进行连续传代培养,并对其E基因的遗传稳定性进行了研究。结果表明,经连续传代60次后病毒E基因趋于稳定,BSF.ZZ-1毒株E蛋白氨基酸位点E21(A→V... 为研究猪乙脑病毒(JEV)分离株遗传基因的稳定性,将JEV分离株BSF.ZZ-1和BSF.ZZ-3在BHK-21细胞上进行连续传代培养,并对其E基因的遗传稳定性进行了研究。结果表明,经连续传代60次后病毒E基因趋于稳定,BSF.ZZ-1毒株E蛋白氨基酸位点E21(A→V)、E200(T→A)、E244(G→E)、E279(M→K)和E426(G→D),以及BSF.ZZ-3毒株的E244(G→E)、E255(F→L)、E285(M→L)、E368(L→S)和E497(N→S)传代后发生稳定点突变。与JEV毒力相关的部分位点如E107、E138、E176、E177和E315遗传稳定性较高,经连续传代后均未发生突变,与疫苗株SA14-14-2相应位点完全一致。但是,另外一些位点的遗传稳定性较差,如BSF.ZZ-3的E279(M→K→M)出现反复突变。这些突变是否与JEV的宿主细胞适应性及毒力变化相关有待进一步研究。 展开更多
关键词 乙脑病毒 BSF.ZZ-1 BSF.ZZ-3 BHK-21细胞系 传代培养 E基因 序列分析
下载PDF
NM-3含药血清对体外胃癌细胞株SGC-7901生长和VEGF及其受体KDR、Flt-1表达的影响 被引量:1
9
作者 宋明全 朱金水 +4 位作者 朱励 张强 李沁 郭花 张卫平 《世界华人消化杂志》 CAS 北大核心 2007年第25期2704-2708,共5页
目的:探讨NM-3含药血清对胃癌SGC-7901细胞的抑制作用.方法:将SGC-7901胃癌细胞分成空白对照组、血清对照组、NM-3含药血清低、中、高剂量实验组共5组.在不同时间段以流式细胞仪检测细胞的凋亡率,分析细胞周期分布;应用逆转录聚合酶链... 目的:探讨NM-3含药血清对胃癌SGC-7901细胞的抑制作用.方法:将SGC-7901胃癌细胞分成空白对照组、血清对照组、NM-3含药血清低、中、高剂量实验组共5组.在不同时间段以流式细胞仪检测细胞的凋亡率,分析细胞周期分布;应用逆转录聚合酶链式反应(RT-PCR)法检测各组胃癌细胞中VEGF及其受体KDR,Flt-1 mRNA的表达.结果:NM-3含药血清3组随着时间的延长凋亡率增高,呈时间剂量依赖性,其高、中剂量组在6h(16.80%±0.40%,25.20%±0.86%)、24h(26.95%±3.25%,43.62%±3.53%)、72 h(39.85%±4.10%,54.35%±5.42%)内的细胞早期凋亡率与空白,血清两个对照组相比有显著性差异(5_34%±0.28%,5.66%±0.72%:6.91%±1.06%,8.90%±0.86%;6.87%±1.24%,8.06%±0.78%;P<0.01).随着NM-3药物剂量的增加,G_0/G_1期细胞增多,而S期及G_2/M期细胞则相应减少.细胞培养72h后,NM-3含药血清高,中,低剂量组与两对照组比较可显著抑制VEGF及其受体KDR,Flt-1 mRNA的表达(P<0.05).在72h后细胞凋亡率,细胞周期以及胃癌细胞中VEGF及其受体KDR,Flt-1 mRNA的表达上,高剂量组与中低剂量组均有明显差异(P<0.05).结论:NM-3含药血清可抑制胃癌组织的血管生长,并可诱导胃癌细胞凋亡. 展开更多
关键词 胃癌 癌细胞株 NM-3 血管内皮生长因子 KDR FLT-1 逆转录聚合酶链式反应
下载PDF
血清IGFBP3、ERCC1与NSCLC患者一线化疗敏感性的关系 被引量:5
10
作者 张秀芳 张军营 王培 《实用癌症杂志》 2021年第5期785-788,共4页
目的探讨血清胰岛素样生长因子结合蛋白3(IGFBP3)、核苷酸切除修复交错互补基因1(ERCC1)表达与非小细胞肺癌(NSCLC)患者一线化疗敏感性的关系。方法选取一线化疗的NSCLC患者107例,在完成4~6个疗程后,根据WHO实体瘤疗效评估结果分为敏感... 目的探讨血清胰岛素样生长因子结合蛋白3(IGFBP3)、核苷酸切除修复交错互补基因1(ERCC1)表达与非小细胞肺癌(NSCLC)患者一线化疗敏感性的关系。方法选取一线化疗的NSCLC患者107例,在完成4~6个疗程后,根据WHO实体瘤疗效评估结果分为敏感组77例、不敏感组30例;对比两组化疗前的血清IGFBP3、ERCC1水平,对比化疗敏感组与不敏感组患者的临床病理学资料;采用Logistic多因素分析影响NSCLC患者一线化疗敏感性的相关因素。结果化疗敏感组患者化疗前的血清IGFBP3、ERCC1水平显著高于不敏感组,差异具有统计学意义(P<0.05);化疗敏感组患者与不敏感组患者的TNM分期、肿瘤分化程度比较,差异具有统计学意义(P<0.05);两组年龄、性别、吸烟、病理类型、病灶直径、淋巴结转移情况差异无统计学意义(P>0.05);经Logistic回归分析,TNM分期增高、分化程度降低、血清IGFBP3水平降低、ERCC1水平降低是NSCLC患者采用一线化疗不敏感的独立危险因素(P<0.05)。结论化疗前的血清IGFBP3、ERCC1水平降低可能是NSCLC患者一线化疗效果不佳的危险因素之一。 展开更多
关键词 胰岛素样生长因子结合蛋白3 核苷酸切除修复交错互补基因1 非小细胞肺癌 一线化疗 敏感性
下载PDF
转录因子Ets-1与β1,3-N-乙酰氨基葡萄糖基转移酶基因启动子结合活性分析(英文)
11
作者 仇灏 徐正荣 +3 位作者 邵雪君 周迎会 徐岚 吴士良 《中国生物化学与分子生物学报》 CAS CSCD 北大核心 2012年第1期61-65,共5页
β1,3-N-乙酰氨基葡萄糖转移酶-2,-8(β3GnT-2,β3GnT-8)共同参与多聚N-乙酰氨基乳糖([Galβ1→4GlcNAcβ1→3]n)的合成,从而使得细胞表面的相应糖链结构延长进而影响细胞的恶性转化.已有研究表明,在全反式维甲酸诱导人白血病细胞株HL-6... β1,3-N-乙酰氨基葡萄糖转移酶-2,-8(β3GnT-2,β3GnT-8)共同参与多聚N-乙酰氨基乳糖([Galβ1→4GlcNAcβ1→3]n)的合成,从而使得细胞表面的相应糖链结构延长进而影响细胞的恶性转化.已有研究表明,在全反式维甲酸诱导人白血病细胞株HL-60分化过程中β3GnT-2,-8的表达上调,但其分子机制不明.本文旨在探讨ATRA诱导HL-60分化过程中,转录因子Ets-1对β3GnT-2,-8表达调控的分子机制.采用10-6mol/L ATRA诱导人白血病细胞株HL-60向粒系分化,RT-PCR检测到细胞中Ets-1的表达明显增加;进一步采用染色质免疫沉淀(ChIP)结合电泳迁移率变动实验(EMSA)检测证实,有活化的Ets-1结合至β3GnT-2/-8基因调控区.以上结果表明,转录因子Ets-1对人白血病细胞株HL-60分化过程中β3GnT-2,-8基因有表达调控作用. 展开更多
关键词 转录因子ETS-1 β1 3-N-乙酰氨基葡萄糖转移酶 HL-60细胞系 全反式维甲酸(ATRA) 染色质免疫沉淀(ChIP) 电泳迁移率变动实验(EMSA)
下载PDF
柔红霉素对HL-60细胞细胞因子信号转导抑制蛋白1、3mRNA表达的影响
12
作者 刘宏涌 彭荷玲 詹文杰 《内科》 2016年第3期355-357,403,共4页
目的探讨柔红霉素(Daunorubicin,DNR)对急性早幼粒细胞白血病(APL)细胞株HL-60细胞中细胞因子信号转导抑制蛋白1(SOCS1)-mRNA、细胞因子信号转导抑制蛋白3(SOCS3)-mRNA表达的影响。方法取HL-60细胞株,设HL-60组、HL-60+DNR组,同时取3例... 目的探讨柔红霉素(Daunorubicin,DNR)对急性早幼粒细胞白血病(APL)细胞株HL-60细胞中细胞因子信号转导抑制蛋白1(SOCS1)-mRNA、细胞因子信号转导抑制蛋白3(SOCS3)-mRNA表达的影响。方法取HL-60细胞株,设HL-60组、HL-60+DNR组,同时取3例正常人外周血白细胞设为NC组。NC及HL-60组未给予干预,HL-60+DNR组为小剂量DNR持续作用HL-60细胞10 d。提取总RNA进行,采用实时荧光定量聚合酶链反应(RT-PCR)法检测SOCS1-mRNA、SOCS3-mRNA转录水平,每组实验重复3次。结果与NC组相比,HL-60组及HL-60+DNR组SOCS1-mRNA转录水平均显著下调(P<0.05),HL-60组下调更明显(P<0.05)。与NC组相比,HL-60组SOCS3-mRNA转录水平显著上调(P<0.05),而HL-60+DNR组上调不明显(P>0.05)。结论 DNR可能通过上调HL-60细胞珠SOCS1及下调其SOCS3的表达,诱导APL细胞的凋亡及促进其成熟,促进急性早幼粒细胞白血病患者病情缓解。 展开更多
关键词 急性早幼粒细胞白血病 HL-60细胞 柔红霉素 SOCS1 SOCS3 细胞凋亡
下载PDF
Caspase-3/Caspase-9活化与皮鳞癌1号方抑制A431细胞生长的关系研究 被引量:1
13
作者 许俏 罗俊 +4 位作者 潘年松 刘英波 丁斗 张学愈 张珏 《安徽医药》 CAS 2015年第1期23-27,共5页
目的研究Caspase-3和Caspase-9活化与皮鳞癌1号方抑制A431细胞生长的关系。方法培养A431细胞,用不同浓度的皮鳞癌1号方分别作用于A431细胞;Hochest染色检测细胞凋亡形态;酶联免疫吸附测定法(ELISA)检测细胞色素C含量;比色法测定Caspase-... 目的研究Caspase-3和Caspase-9活化与皮鳞癌1号方抑制A431细胞生长的关系。方法培养A431细胞,用不同浓度的皮鳞癌1号方分别作用于A431细胞;Hochest染色检测细胞凋亡形态;酶联免疫吸附测定法(ELISA)检测细胞色素C含量;比色法测定Caspase-3和Caspase-9活性。结果 Hochest33258染色可见皮鳞癌1号方组A431细胞发生核固缩、凋亡小体等典型的凋亡形态学特征;与对照组比较,Cytc、Caspase-3、Caspase-9表达增加。结论 Caspase-3和Caspase-9的活化与皮鳞癌1号方可诱导A431发生凋亡有关。 展开更多
关键词 皮鳞癌1号方 A431细胞 凋亡 CASPASE-3 CASPASE-9
下载PDF
表皮生长因子对前列腺癌PC-3细胞分泌内皮素-1的影响 被引量:1
14
作者 姜彦飞 贾瑞鹏 许露伟 《南京医科大学学报(自然科学版)》 CAS CSCD 北大核心 2007年第4期360-363,共4页
目的:探讨表皮生长因子(epidermal growth factor,EGF)对激素非依赖性前列腺癌(hormone refractory prostate cancer,HRPC)PC-3细胞中内皮素-1(endothelin-1,ET-1)分泌和mRNA表达的影响。方法:EGF干预后,RT-PCR测定PC-3中ET-1mRNA的表达... 目的:探讨表皮生长因子(epidermal growth factor,EGF)对激素非依赖性前列腺癌(hormone refractory prostate cancer,HRPC)PC-3细胞中内皮素-1(endothelin-1,ET-1)分泌和mRNA表达的影响。方法:EGF干预后,RT-PCR测定PC-3中ET-1mRNA的表达;放免检测ET-1蛋白分泌;不同剂量EGF干预后,放免检测ET-1分泌量的变化。结果:EGF干预后,ET-1mRNA表达上调,ET-1蛋白分泌增加,与对照组比较,差异有显著性(P<0.05);不同剂量EGF干预后,ET-1分泌随EGF浓度增加而增加,单因素方差分析表明,不同剂量的EGF对PC-3细胞ET-1分泌的影响不同,差异具有显著性(P<0.05)。结论:EGF可上调激素非依赖性前列腺癌PC-3细胞中ET-1mRNA表达及蛋白分泌,在前列腺癌的进展中起协同作用,为HRPC的治疗提供了分子生物学基础。 展开更多
关键词 内皮素-1 表皮生长因子 激素非依赖性前列腺癌 PC-3细胞
下载PDF
miR-138-5p通过PDK1对人肺癌细胞系H23生物学行为的影响 被引量:3
15
作者 刘利 李婷婷 冯佳 《临床肺科杂志》 2022年第4期576-580,585,共6页
目的探讨微小RNA-138-5p(miR-138-5p)通过3-磷酸肌醇依赖性蛋白激酶1(PDK1)对人肺腺癌细胞系H23生物学行为的影响。方法以肺腺癌细胞系H23作为研究对象,分别转染miR-NC(对照组)或miR-138-5p(实验组);qRT-PCR与Western blot法检测miR-138... 目的探讨微小RNA-138-5p(miR-138-5p)通过3-磷酸肌醇依赖性蛋白激酶1(PDK1)对人肺腺癌细胞系H23生物学行为的影响。方法以肺腺癌细胞系H23作为研究对象,分别转染miR-NC(对照组)或miR-138-5p(实验组);qRT-PCR与Western blot法检测miR-138-5p、PDK1 mRNA在转染后人肺腺癌细胞系H23中表达水平;双荧光素酶报告基因检测miR-138-5p及基因PDK1之间的靶向关系;MTT法、划痕实验、Transwell实验检测增殖、迁移与侵袭能力。结果qRT-PCR检测H23细胞转染后miR-138-5p mRNA表达水平升高,PDK1 mRNA与蛋白表达下调,荧光素酶报告基因实验提示miR-138-5p可与PDK1的3’-UTR直接结合,与PDK1存在靶向关系。miR-138-5p可抑制H23细胞增殖、迁移和侵袭能力。结论miR-138-5p可通过靶向干扰PDK1抑制人肺腺癌细胞系H23细胞的增殖、迁移与侵袭能力,提示miR-138-5p与PDK1可能是治疗肺癌的潜在靶点。 展开更多
关键词 微小RNA-138-5p 3-磷酸肌醇依赖性蛋白激酶1 人肺腺癌细胞系H23 增殖 迁移 侵袭
下载PDF
Apoptotic effect and mechanisms of AHPN on human skin malignant melanoma cell A375 被引量:2
16
作者 Min Pan Zhen-hui Peng Sheng-xiang Xiao Jian-wen Ren Yan Liu Xiao-li Li Zheng-xiao Li 《Journal of Nanjing Medical University》 2008年第1期18-22,共5页
Objective: To study apoptotic effects of synthetic retinoic acid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid(AHPN) on human skin malignant melanoma A375 cells in comparison with the natural ... Objective: To study apoptotic effects of synthetic retinoic acid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid(AHPN) on human skin malignant melanoma A375 cells in comparison with the natural ligand all-trans-retinoic acid(ATRA) in vitro and the mechanisms related to the actions of AHPN. Methods:MTT assay was used to determine the anti-proliferative effects of AHPN and ATRA on A375 cells. Flow cytometry was performed to investigate the influence of AHPN and ATRA on cell cycle and cell apoptosis. In addition, transfection and luciferase activity assays were employed to explore the mechanisms of how AHPN executes its proapoptotic function. Results:Firstly, AHPN promoted apoptosis and GI arrest in A375 cells compared with ATRA. Secondly, the activity of NF-K B in A375 cells treated with AHPN increased 2-3 times compared with solvent DMSO treatment. Conclusion:AHPN, in comparison with ATRA, is a more effective alternative for therapy of malignant melanoma. The potentially proapoptotic function of AHPN requires activation of NF-K B. 展开更多
关键词 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid(AHPN) ATRA a375 cell line apoptosis NF-K B
下载PDF
Effects of fulvestrant on biological activity and Wnt expression in rat GH3 cells 被引量:1
17
作者 Jiwei Bai Yan Wang +1 位作者 Chuzhong Li Yazhuo Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第4期283-289,共7页
The present study investigated the influence of anti-estrogen treatment (fulvestrant) on pituitary adenoma cell line GH3 biological activity, the estrogen receptor a pathway, the WnT pathway, and mechanisms of decre... The present study investigated the influence of anti-estrogen treatment (fulvestrant) on pituitary adenoma cell line GH3 biological activity, the estrogen receptor a pathway, the WnT pathway, and mechanisms of decreased Wnt inhibitory factor-1 expression in GH3 cells. Results showed that fulvestrant suppressed GH3 cell proliferation and reduced hormone secretion in a dose-dependent manner. Estrogen receptor a and Wnt4 expression decreased, but Wnt inhibitory factor-1 expression increased in a dose-dependent manner following fulvestrant treatment, and β-catenin expression remained unchanged. Inhibitors of DNA methylation and histone modification upregulated Wnt inhibitory factor-1 expression. Results suggested that fulvestrant suppressed biological activity of GH3 cells via the estrogen receptor a and Wnt pathways. These results suggested that decreased Wnt inhibitory factor-1 expression in GH3 cells played a role in epigenetic mechanisms. Anti-estrogen therapies could provide novel treatments for growth hormone adenomas. 展开更多
关键词 β-catenin ESTROGEN estrogen receptor a GH3 cell line Wnt inhibitory factor-1 Wnt4
下载PDF
美洲大蠊提取物CⅡ-3对MFC荷瘤小鼠抑瘤机制的~1H-NMR代谢组学研究 被引量:4
18
作者 厉颖 陶柱萍 +7 位作者 常旭 欧红利 江伦 李灿委 唐艳隆 周玥 白丽 高鹏飞 《中国药房》 CAS 北大核心 2020年第12期1446-1451,共6页
目的:初步研究美洲大蠊提取物CⅡ-3对上皮肿瘤细胞MFC荷瘤小鼠的抑瘤机制。方法:将Balb/c小鼠随机分为模型组(生理盐水20 mL/kg)和CⅡ-3组(200 mg/kg),每组6只。在小鼠右侧腋下注射MFC细胞悬液0.2 mL后,于次日灌胃相应药物,每日1次,连续... 目的:初步研究美洲大蠊提取物CⅡ-3对上皮肿瘤细胞MFC荷瘤小鼠的抑瘤机制。方法:将Balb/c小鼠随机分为模型组(生理盐水20 mL/kg)和CⅡ-3组(200 mg/kg),每组6只。在小鼠右侧腋下注射MFC细胞悬液0.2 mL后,于次日灌胃相应药物,每日1次,连续10 d。末次给药24 h后,在测量瘤体大小的基础上,采用氢-1核磁共振技术(~1H-NMR)并结合非监督型主成分分析(PCA)、监督型偏最小二乘法-判别分析(PLS-DA)和正交偏最小二乘法-判别分析(OPLS-DA),比较两组荷瘤小鼠肝组织的代谢谱并分析差异性代谢物,探索CⅡ-3抑瘤作用的潜在机制。结果:与模型组比较,CⅡ-3组荷瘤小鼠的瘤体明显减小;两组小鼠的~1H-NMR图谱存有差异;结合非监督型PCA、监督型PLS-DA、OPLS-DA结果,共确定了肝组织潜在差异性代谢物6个,分别为糖原(升高)、丙酮酸(降低)、精氨酸(降低)、羟脯氨酸(升高)、肌苷(升高)、烟酰胺(升高),主要归属于精氨酸代谢、能量代谢和核酸代谢。结论:CⅡ-3对MFC荷瘤小鼠的抑瘤作用可能与调节精氨酸代谢、能量代谢和核酸代谢有关。 展开更多
关键词 美洲大蠊提取物CⅡ-3 上皮肿瘤细胞MFC 代谢组学 氢-1核磁共振技术 小鼠
下载PDF
长链非编码RNA FTH1P3靶向miR-218降低人肺癌顺铂耐药细胞对顺铂的化疗敏感性 被引量:3
19
作者 李正雄 王雅棣 《中国肿瘤临床》 CAS CSCD 北大核心 2021年第12期595-602,共8页
目的:研究长链非编码RNA铁蛋白重链1假基因3(ferritin heavy chain 1 pseudogene 3,FTH1P3)对人肺癌顺铂(cisplatin,DDP)耐药细胞株(A549/DDP)DDP化疗敏感性的影响,并探究其潜在的分子机制。方法:采用荧光定量PCR检测FTH1P3与miR-218在A... 目的:研究长链非编码RNA铁蛋白重链1假基因3(ferritin heavy chain 1 pseudogene 3,FTH1P3)对人肺癌顺铂(cisplatin,DDP)耐药细胞株(A549/DDP)DDP化疗敏感性的影响,并探究其潜在的分子机制。方法:采用荧光定量PCR检测FTH1P3与miR-218在A549和A549/DDP细胞中的表达。采用MTT法、流式细胞术、Hoechst 33258染色及CASP3活性试验评估细胞对DDP化疗敏感性的影响。采用荧光素酶报告基因和RNA蛋白免疫沉淀试验分析FTH1P3对miR-218的调控作用。结果:与A549细胞相比,A549/DDP细胞中FTH1P3表达上调,而miR-218表达下调(P<0.05)。与si-NC相比,si-FTH1P3增加A549/DDP细胞对DDP的化疗敏感性,表现为半抑制浓度(IC_(50))降低,多药耐药关联蛋白1(multidrug resistance-associated protein 1,MRP1)和ATP结合家族亚家族B成员1(ATP binding cassette subfamily B member 1,ABCB1)mRNA表达下调,细胞生长能力降低、凋亡增加及CASP3活性升高(P<0.05)。FTH1P3直接结合miR-218并抑制其表达(P<0.05)。与NC抑制物相比,miR-218抑制物能够逆转经si-FTH1P3处理的A549/DDP细胞对DDP的化疗敏感性(P<0.05)。结论:FTH1P3在A549/DDP细胞中表达上调,FTH1P3降低A549/DDP细胞对DDP的化疗敏感性,其机制与miR-218表达下调有关。 展开更多
关键词 铁蛋白重链1假基因3 A549/DDP细胞系 MIR-218 化疗敏感性
下载PDF
阿司匹林通过抑制STAT3磷酸化下调MCL-1和VEGF mRNA和蛋白表达促进胆囊癌细胞凋亡、抑制增殖 被引量:2
20
作者 李皇保 周俊 +2 位作者 赵凤庆 吴晓俊 闵捷 《肝胆胰外科杂志》 CAS 2021年第3期158-164,共7页
目的探讨阿司匹林对人胆囊癌细胞株GBC-SD细胞凋亡及增殖的影响及其潜在机制。方法采用MTT法检测不同浓度梯度及作用时间下阿司匹林对GBC-SD细胞增殖的影响,流式细胞术检测阿司匹林对细胞凋亡的影响;Real-time PCR检测GBC-SD细胞中信号... 目的探讨阿司匹林对人胆囊癌细胞株GBC-SD细胞凋亡及增殖的影响及其潜在机制。方法采用MTT法检测不同浓度梯度及作用时间下阿司匹林对GBC-SD细胞增殖的影响,流式细胞术检测阿司匹林对细胞凋亡的影响;Real-time PCR检测GBC-SD细胞中信号转导和转录激活因子3(STAT3)、髓细胞白血病因子-1(MCL-1)、血管内皮生长因子(VEGF)的mRNA表达水平,Western blotting检测STAT3、磷酸化信号转导与转录激活因子3(pSTAT3)、MCL-1、VEGF的蛋白表达情况。结果阿司匹林对GBC-SD细胞增殖的抑制作用呈浓度依赖及时间依赖,与对照组相比差异有统计学意义(P<0.05)。阿司匹林可促进GBC-SD细胞凋亡。阿司匹林可下调MCL-1和VEGF的mRNA表达水平,与对照组相比差异有统计学意义(P<0.05),但对STAT3 mRNA表达水平无明显影响(P>0.05)。阿司匹林可下调pSTAT3、MCL-1、VEGF的蛋白表达水平(P<0.05),但对STAT3蛋白表达水平无明显影响(P>0.05);使用STAT3激动剂后,STAT3、pSTAT3、MCL-1、VEGF的蛋白表达水平高于未使用激动剂组(P<0.05),在激动剂组加入阿司匹林后,pSTAT3、MCL-1、VEGF的蛋白表达水平下调(P<0.05),但高于无激动剂组(P<0.05)。结论在GBC-SD细胞中,阿司匹林通过抑制STAT3磷酸化下调MCL-1、VEGF的mRNA及蛋白表达水平,从而促进胆囊癌细胞的凋亡,抑制增殖。 展开更多
关键词 胆囊癌 GBC-SD细胞株 阿司匹林 信号转导与转录激活因子3(STAT3) 髓细胞白血病因子-1(MCL-1) 血管内皮生长因子(VEGF)
下载PDF
上一页 1 2 3 下一页 到第
使用帮助 返回顶部