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Effect of Mono-2-ethyhexyl Phthalate on DNA Methylation in Human Prostate Cancer lncap Cells

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Biomedical and Environmental Sciences 2017年第9期30卷 641-648页

作者： WU Jian Hui CHEN Jiao WANG Yong XIA Bin WANG Rong ZHAO Yan WANG Qin Xia SONG Qi YAO Shun Heng ZHANG Yun Hui SUN Zu Yue National Evaluation Centre for the Toxicology of Fertility Regulating Drug Department of Pharmacology and ToxicologyShanghai Institute of Planned Parenthood ResearchShanghai 200032China Key Laboratory of Reproduction Regulation of NPFPC Shanghai 200032China Reproductive and Developmental Research Institute of Fudan University ShanghaiShanghai 200032China Division of Health Risk Factors Surveillance and Control Shanghai Municipal Center for Disease Control and PreventionShanghai 200336China Key Laboratory of Public Health Safety Ministry of EducationSchool of Public HealthFudan UniversityShanghai 200032China

Objective To evaluate whether mono（2‐ethylhexyl） phthalate（MEHP） affects genomic DNA methylation and the methylation status of some specific genes such as patched gene（PTCH） and smoothened gene（SMO） in lncap cells. Methods lncap cells were treated with MEHP（0, 1, 5, 10, and 25 μmol/L） for 3 days. An ELISA assay was preformed to detect genomic methylation, including 5‐methylcytosine（5‐mC） and 5‐hydroxymethylcytosine（5‐hmC） content. A pyrosequencing assay was applied to assess DNA methylation in PTCH and SMO gene promoters. The correlation between DNA methylation and gene expression was assessed. Results The proportion of cytosines with 5‐mC methylation in lncap cells was significantly decreased by MEHP（1, 5, 10, and 25 μmol/L） in a dose‐dependent manner（P 〈 0.01）. For genes in the Hedgehog pathway, there was no significant MEHP concentration‐dependent difference in the DNA methylation of PTCH and SMO. Conclusion MEHP might affect the progression of prostate cancer through its effect on global DNA methylation.

关键词： Mono(2‐ethyhexyl) phthalate lncap Genomic Methylation PTCH SMO

Chimeric molecules facilitate the degradation of androgen receptors and repress the growth of lncap cells

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Asian Journal of Andrology 2009年第1期11卷 119-126页

作者： Yue-Qing Tang Bang-Min Han Xin-Quan Yao Yan Hong Yan Wang Fu-Jun Zhao Sheng-Qiang Yu Xiao-Wen Sun Shu-Jie Xia Department of Urology Shanghai First People＇s Hospital Institute of Urology Department of Urology Wujiang Third People＇s Hospital Suzhou 215228 China Department of Immunology Shanghai Jiao Tong University Shanghai 200025 China

Post-translational degradation of protein plays an important role in cell life. We employed chimeric molecules （dihydrotestosterone-based proteolysis-targeting chimeric molecule [DHT-PROTAC]） to facilitate androgen receptor （AR） degradation via the ubiquitin-proteasome pathway （UPP） and to investigate the role of AR in cell proliferation and viability in androgen-sensitive prostate cancer cells. Western blot analysis and immunohistochemistry were applied to analyse AR levels in lncap cells after DHT-PROTAC treatment. Cell counting and the 3-（4,5-dimethylthiazol-2-yl）-2,5- diphenyl tetrazolium bromide （MTT） cell viability assay were used to evaluate cell proliferation and viability after AR elimination in both lncap and PC-3 cells. AR was tagged for elimination via the UPP by DHT-PROTAC, and this could be blocked by proteasome inhibitors. Degradation of AR depended on DHT-PROTAC concentration, and either DHT or an ALAPYIP-（arg）8 peptide could compete with DHT-PROTAC. Inhibition of cell proliferation and decreased viability were observed in lncap cells, but not in PC-3 or 786-0 cells after DHT-PROTAC treatment. These data indicate that AR elimination is facilitated via the UPP by DHT-PROTAC, and that the growth of lncap cells is repressed after AR degradation.

关键词： androgen receptor lncap prostate cancer proteolysis ubiquitin

Dioscin-induced Apoptosis of Human lncap Prostate Carcinoma Cells through Activation of Caspase-3 and Modulation of Bcl-2 Protein Family

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2014年第1期34卷 125-130页

作者：陈静李辉敏张学农熊朝梅阮金兰 Key Laboratory of Natural Medicinal Chemistry and Resources Evaluation of Hubei Province School of Pharmacy Tongji Medical College Huazhong University of Science and Technology School of Basic Medical Science Jiujiang University Department of Pharmacy Yichang Central People’s Hospital the First College of Clinical Medical Science China Three Gorges University

Dioscin is a natural steroid saponin derived from several plants, showing potent anti-cancer effect against a variety of tumor cell lines. In the present study, we investigated the anti-cancer activity of dioscin against human lncap cells, and evaluated the possible mechanism involved in its antineoplastic action. It was found that dioscin（1, 2 and 4 μmol/L） could significantly inhibit the viability of lncap cells in a time- and concentration-dependent manner. Flow cytometry revealed that the apoptosis rate was increased after treatment of lncap cells with dioscin for 24 h, indicating that apoptosis was an important mechanism by which dioscin inhibited cancer. Western blotting was employed to detect the expression of caspase-3, Bcl-2 and Bax in lncap cells. The expression of cleaved caspase-3 was significantly increased, and meanwhile procaspase-3 was markedly decreased. The expression of anti-apoptotic protein Bcl-2 was down-regulated, whereas the pro-apoptotic protein Bax was up-regulated. Moreover, the Bcl-2/Bax ratio was drastically decreased. These results suggested that dioscin possessed potential anti-tumor activity in human lncap cells through the apoptosis pathway, which might be associated with caspase-3 and Bcl-2 protein family.

关键词： dioscin lncap anti-tumor apoptosis pathway capsase-3 Bcl-2 protein family

A Comparative Study on Proteomics between lncap and DU145 Cells by Quantitative Detection and SELDI Analysis

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2008年第2期28卷 174-178页

作者：孙伟桂叶章群米振国史天良韩存芝郭素堂 Department of Urology Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology Wuhan 430030 China Shanxi Cancer Research Institute Taiyuan 030013 China

The differences in intracellular and extracellular protein expressions between human prostate cancer lines lncap and DU145 were examined, The proteins of the two cell lines were extracted and condensed by using protein extraction kits. And the intracellular and extracellular proteins were quantitatively detected on a micro-plate reader by using bicinchoninic acid （BCA） method. The proteins in cell culture fluid were qualitatively assayed by SELDI-TOF-MS, The results showed that the intracellular protein contents of lncap cells were extremely higher than those of DU145 cells. After serum-free culture, both intracellular and extracellular protein contents of lncap and DU145 were decreased to some extent. And the intracellular proteins were decreased by 5% in lncap and by 36% in DU145 respectively, while the extracellular proteins were decreased by 89% in lncap and 96% in DU145 respectively. SELDI assay revealed that there were 5 marker proteins in lncap and 6 in DU145. Although both lncap and DU145 cell lines originated from human prostate cancer, they had some differences in protein expression.

关键词： prostate cancer lncap DU145 protein quantitative and qualitative study SELDI-TOF-MS

lncap衍生的雄激素非依赖型前列腺癌细胞系C4-2对辐射的应答反应

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Asian Journal of Andrology 2010年第3期12卷 405-414,I0011页

作者： Bang-Xiang Xie Hui Zhang Lan Yu Jian Wang Bo Pang Rui-Qin Wu Xiao-Long Qian Shan-Hu Li Qing-Guo Shi Le-Le Wang Jian-Guang Zhou Laboratory of Molecular Biology of Medicine Beijing Institute of Bioteehnology Beijing 100850 China National Institute for Viral Disease Control and Prevention Chinese Center for Disease Control and Prevention Beijing 100052 China

Radiation therapy is a relatively effective therapeutic method for localized prostate cancer （PCa） patients. However, radioresistance occurs in nearly 30% of patients treated with potentially curative doses. Therapeutic synergy between radiotherapy and androgen ablation treatment provides a promising strategy for improving the clinical outcome. Accordingly, the androgen deprivation-induced signaling pathway may also mediate radiosensitivity in PCa cells. The C4-2 cell line was derived from the androgen-sensitive lncap parent line under androgen-depleted condition and had acquired androgen-refractory characteristics. In our study, the response to radiation was evaluated in both lncap and C4-2. Results showed that C4-2 cells were more likely to survive from irradiation and appeared more aggressive in their resistance to radiation treatment compared with lncap, as measured by clonogenic assays and cell viability and cell cycle analyses. Gene expression analyses revealed that a set of genes involved in cell cycle arrest and DNA repair were differentially regulated in lncap and C4-2 in response to radiation, which was also consistent with the radiation-resistant property observed in C4-2 cells. These results strongly suggested that the radiation-resistant property may develop with progression of PCa to androgen- independent status. Not only can the lncap and C4-2 PCa progression model be applied for investigating androgen-refractory progression, but it can also be used to explore the development of radiation resistance in PCa.

关键词： lncap C4-2 prostate cancer radiation response

恩杂鲁胺对前列腺癌lncap细胞衰老的影响及其机制研究

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临床医学进展 2023年第5期13卷 7783-7789页

作者：冯诗尧李良姚锴闫海新张志辉谢栋栋安徽医科大学第二附属医院泌尿外科安徽合肥

探讨雄激素受体抑制剂恩杂鲁胺对人前列腺癌lncap细胞衰老的影响。使用CCK8实验检测lncap细胞对恩杂鲁胺的IC50,将加入等体积DMSO的lncap细胞定义为对照组,lncap细胞以IC50浓度的恩杂鲁胺慢性处理1个月设为实验组。β-半乳糖苷酶染色试... 详细信息

探讨雄激素受体抑制剂恩杂鲁胺对人前列腺癌lncap细胞衰老的影响。使用CCK8实验检测lncap细胞对恩杂鲁胺的IC50,将加入等体积DMSO的lncap细胞定义为对照组,lncap细胞以IC50浓度的恩杂鲁胺慢性处理1个月设为实验组。β-半乳糖苷酶染色试剂盒检测细胞衰老;克隆形成实验检测细胞增殖;蛋白免疫印记实验检测雄激素受体,衰老标志蛋白的表达情况和信号转导机制。结果显示lncap细胞在1 μM (IC50)剂量恩杂鲁胺慢性暴露后,雄激素受体被抑制,细胞发生衰老,表现为β-半乳糖苷酶染色增多,衰老标记蛋白p16,p21表达上调。通过对信号转导研究发现,实验组中YAP1磷酸化水平降低,入核增多,YAP1可能是恩杂鲁胺致lncap细胞衰老的关键信号。

关键词：恩杂鲁胺前列腺癌 lncap 细胞衰老 YAP1

复方中药紫龙金对前列腺癌细胞系lncap的体外作用

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中国中西医结合杂志 2004年第7期24卷 621-624页

作者：李学松梁云燕王代树谢贤和师长进陈捷孙国锋周利群薛兆英那彦群郭应禄北京大学第一医院 100034 北京大学肿瘤医院北京大学泌尿外科研究所北京市肿瘤防治研究所福建医科大学协和临床医学院

目的探讨复方中药紫龙金 (简称紫龙金 )对雄激素依赖型人前列腺癌细胞系lncap的体外作用机制。方法应用MTT法、流式细胞术和显微荧光术测定紫龙金对lncap的增殖、细胞周期分布和诱导凋亡的影响 ,应用RT PCR方法检测前列腺特异性抗原基因... 详细信息

目的探讨复方中药紫龙金 (简称紫龙金 )对雄激素依赖型人前列腺癌细胞系lncap的体外作用机制。方法应用MTT法、流式细胞术和显微荧光术测定紫龙金对lncap的增殖、细胞周期分布和诱导凋亡的影响 ,应用RT PCR方法检测前列腺特异性抗原基因 (PSA)和雄激素受体 (AR) ,凋亡相关基因bcl 2和bax蛋白表达的影响 ;应用Westernblot方法测定对bcl 2和bax蛋白表达的影响。结果紫龙金对lncap细胞具有时间和剂量依赖性增殖抑制、G0 /G1期阻滞和诱导凋亡作用 ,作用 72h时IC50 为 0 .79mg/ml;紫龙金可以下调前列腺特异性标志基因PSA、AR和凋亡相关基因bcl 2的表达 ,降低bcl 2蛋白表达 ,对bax蛋白表达无明显作用。结论紫龙金可以通过抑制lncap细胞增殖、G0 /G1期阻滞、诱导凋亡、下调PSA、AR和bcl 2基因表达 ,降低bcl 2蛋白表达等作用机制发挥抗肿瘤作用。

关键词：复方中药紫龙金前列腺癌癌细胞系 lncap 体外作用肿瘤

依立雄胺对前列腺癌细胞(lncap)前列腺特异性抗原和Bcl-2蛋白体外表达的抑制作用

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中国药理学与毒理学杂志 2003年第1期17卷 29-34页

作者：钟恩宏孙祖越顾正吴建辉朱焰何桂林刘桂明上海市计划生育科学研究所计划生育药具国家重点实验室中国生育调节药物毒理检测中心上海200032

目的　为研究依立雄胺治疗前列腺癌的可能性及可能机制 ,探讨依立雄胺体外对人激素依赖型前列腺癌细胞 (lncap)生长及前列腺特异性抗原(PSA)与Bcl 2蛋白表达的作用。方法　用 5 ,15和4 5 μmol·L- 1的依立雄胺作用lncap细胞 3d或 7d后 ... 详细信息

目的　为研究依立雄胺治疗前列腺癌的可能性及可能机制 ,探讨依立雄胺体外对人激素依赖型前列腺癌细胞 (lncap)生长及前列腺特异性抗原(PSA)与Bcl 2蛋白表达的作用。方法　用 5 ,15和4 5 μmol·L- 1的依立雄胺作用lncap细胞 3d或 7d后 ,相差显微镜进行细胞形态学观察 ;台盼蓝染色活细胞计数 ,绘制 7d的生长曲线 ;应用流式细胞仪分析依立雄胺对lncap细胞凋亡的影响 ;应用免疫组化ABC比较经依立雄胺作用后lncap细胞PSA与Bcl 2蛋白的表达强度。结果　 4 5 μmol·L- 1的依立雄胺作用lncap细胞 3d后 ,可使其明显的皱缩脱壁 ,部分细胞膜破裂。在 5 ,15和 4 5 μmol·L- 1的依立雄胺作用 7d后 ,可明显抑制lncap细胞的生长 ,抑制率分别达 4 0 .0 % ,4 7.4 %和 5 4 .3% ;流式细胞仪分析显示上述浓度的依立雄胺可诱导细胞凋亡 ,凋亡率分别为 3.5 % ,15 .8%和 2 5 .0 % ,而对照组为2 .2 % ;免疫组化分析表明依立雄胺可降低lncap细胞PSA和Bcl 2蛋白的表达。结论　在上述浓度下依立雄胺可特异性的抑制lncap细胞的生长和PSA与Bcl

关键词：依立雄胺凋亡免疫组化细胞株 lncap 前列腺蛋白表达

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lncap前列腺癌小鼠原位接种模型的建立

LNCaP前列腺癌小鼠原位接种模型的建立