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食管癌多倍体肿瘤巨细胞DNA定量分析
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作者 张国栋 任旖琳 王卫 《临床与实验病理学杂志》 CAS 北大核心 2024年第2期209-212,共4页
目的探讨CD133阳性肿瘤干细胞(cancer stem cells,CSCs)与食管癌多倍体肿瘤巨细胞(polyploid giant cancer cells,PGCCs)DNA含量之间的关系。方法采用紫杉醇诱导食管癌细胞产生PGCCs,免疫细胞化学技术检测CSCs标志物CD133、CD44和c-Myc... 目的探讨CD133阳性肿瘤干细胞(cancer stem cells,CSCs)与食管癌多倍体肿瘤巨细胞(polyploid giant cancer cells,PGCCs)DNA含量之间的关系。方法采用紫杉醇诱导食管癌细胞产生PGCCs,免疫细胞化学技术检测CSCs标志物CD133、CD44和c-Myc的表达;磁珠分选未经紫杉醇处理的食管癌细胞,获得CD133+和CD133-细胞亚群,对两个亚群进行细胞DNA定量分析。结果紫杉醇诱导食管癌产生PGCCs,与未经紫杉醇处理细胞相比,PGCCs高表达CSCs标志物CD133、CD44和c-Myc。在未经紫杉醇处理的细胞中,PGCCs富集在CD133+细胞亚群;细胞DNA定量分析结果表明,八倍体及以上的PGCCs主要富集于CD133+细胞亚群。结论八倍体及以上的食管癌PGCCs是CSCs的一个亚群,PGCCs可为食管癌患者耐药、复发和预后提供重要参考,并为临床治疗食管癌提供一种新的方向和思路。 展开更多
关键词 食管肿瘤 pgccs 肿瘤干细胞 CD133 八倍体
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k次Petersen连通圈网络
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作者 李倩雅 张治成 佟永鹏 《应用数学进展》 2024年第5期2045-2052,共8页
互连网络是超级计算机体系结构的重要组成部分。文中利用正则图连通圈网络模型,设计出了新模型k次Petersen连通圈网络PGCC(k),它是3正则3连通的,且具有其他好的性质。本文对它的圈因子分解、Hamilton性和一些基本性质进行了研究,并证明... 互连网络是超级计算机体系结构的重要组成部分。文中利用正则图连通圈网络模型,设计出了新模型k次Petersen连通圈网络PGCC(k),它是3正则3连通的,且具有其他好的性质。本文对它的圈因子分解、Hamilton性和一些基本性质进行了研究,并证明了PGCC(1)可分解为边不交的两个等长圈和一个完美对集的并。 展开更多
关键词 互连网络 HAMILTON图 完美对集 圈因子 pgcc(k)
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VEGF-CDC42-P38MAPK参与调控多倍体肿瘤巨细胞(PGCCs)及其子代细胞的迁移侵袭
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作者 付俊杰 郑敏英 张诗武 《南开大学学报(自然科学版)》 CAS CSCD 北大核心 2022年第2期13-20,共8页
通过提取总蛋白和细胞质和核蛋白,比较LoVo和HCT116对照细胞和450μmol/L CoCl;处理后细胞中VEGF、CDC42和p38 MAPK的表达水平,实验结果显示,与对照组相比,处理组细胞中VEGF、CDC42和p38 MAPK的总蛋白水平升高.通过免疫细胞化学检测CoCl... 通过提取总蛋白和细胞质和核蛋白,比较LoVo和HCT116对照细胞和450μmol/L CoCl;处理后细胞中VEGF、CDC42和p38 MAPK的表达水平,实验结果显示,与对照组相比,处理组细胞中VEGF、CDC42和p38 MAPK的总蛋白水平升高.通过免疫细胞化学检测CoCl;处理前后细胞中VEGF、CDC42、p38 MAPK的表达及定位,结果显示VEGF、CDC42位于细胞质中的表达,p38 MAPK位于细胞质和细胞核中的表达.通过瞬时转染小干扰RNA来敲低CDC42的表达,检测VEGF和p38 MAPK的蛋白表达并通过平板克隆形成试验、Transwell迁移和侵袭试验比较处理组细胞在敲低CDC42前后的增殖、迁移和侵袭能力.实验结果表明CDC42敲低后,CoCl;处理后细胞的迁移和侵袭能力下降.本实验证明PGCCs及其子代细胞的高侵袭和迁移能力与VEGF-CDC42-p38 MAPK信号通路有关. 展开更多
关键词 多倍体肿瘤巨细胞(pgccs) CDC42 VEGF p38 MAPK 细胞迁移
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Acetylated-PPARγexpression is regulated by different P53 genotypes associated with the adipogenic differentiation of polyploid giant cancer cells with daughter cells 被引量:1
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作者 Kexin Zhang Xiaohui Yang +2 位作者 Minying Zheng Yidi Ning Shiwu Zhang 《Cancer Biology & Medicine》 SCIE CAS CSCD 2023年第1期56-76,共21页
Objective:Polyploid giant cancer cells(PGCCs)with daughter cells express epithelial–mesenchymal transition(EMT)-associated proteins.Highly malignant tumor cells with EMT properties can transdifferentiate into mature ... Objective:Polyploid giant cancer cells(PGCCs)with daughter cells express epithelial–mesenchymal transition(EMT)-associated proteins.Highly malignant tumor cells with EMT properties can transdifferentiate into mature tumor cells.In this study,we elucidated the potential for,and underlying mechanism of,adipogenic differentiation of PGCCs with daughter cells(PDCs).Methods:Cobalt chloride was used to induce PGCC formation in HEY(wild-type P53)and MDA-MB-231(mutant P53)cells;these cells were then cultured in adipogenic differentiation medium.Oil red O staining was used to confirm adipogenic differentiation,and the cell cycle was detected with flow cytometry.The expression of adipogenic differentiation-associated proteins and P300 histone acetyltransferase activity were compared before and after adipogenic differentiation.Animal xenograft models were used to confirm the adipogenic differentiation of PDCs.Results:PDCs transdifferentiated into functional adipocytes.Two different cell cycle distributions were observed in PDCs after adipogenic differentiation.The expression levels of PPARγ,Ace-PPARγ,and Ace-P53 were higher in PDCs after adipogenic differentiation than in cells before adipogenic differentiation.Ace-PPARγand FABP4 expression increased in HEY cells and decreased in MDA-MB-231 PDCs after p53 knockdown.A485 treatment increased Ace-P53,Ace-PPARγ,and FABP4 expression in HEY PDCs by inhibiting SUMOylation of P53.In MDA-MB-231 PDCs,A485 treatment decreased Ace-P53,Ace-PPARγ,and FABP4 expression.Animal experiments also confirmed the adipogenic differentiation of PDCs.Conclusions:Acetylation of P53 and PPARγplays an important role in the adipogenic differentiation of PDCs. 展开更多
关键词 pgccs adipogenic differentiation PPARΓ post-translational modification P53 genotype
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从2011年美国总统绿色化学挑战奖谈绿色涂料
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作者 张变香 吴群 +2 位作者 常姣 魏保利 闫光红 《山西化工》 2012年第2期22-25,共4页
简述了2011年美国总统绿色化学挑战奖的更绿色化学品奖项,阐述了当前4种绿色涂料的研究现状及发展趋势,并展望了绿色涂料的发展前景。
关键词 总统绿色化学挑战奖(pgcc) 绿色涂料 高固体分涂料 粉末涂料 水性涂料 辐射固化涂料
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Cancer genes and cancer stem cells in tumorigenesis:Evolutionary deep homology and controversies 被引量:1
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作者 Vladimir F.Niculescu 《Genes & Diseases》 SCIE 2022年第5期1234-1247,共14页
In the past,contradictory statements have been made about the age of cancer genes.While phylostratigraphic studies suggest that cancer genes emerged during the transitional period from unicellularians(UC)to early meta... In the past,contradictory statements have been made about the age of cancer genes.While phylostratigraphic studies suggest that cancer genes emerged during the transitional period from unicellularians(UC)to early metazoans(EM),life cycle studies suggest that they arose earlier.This controversy could not be resolved.Phylostratigraphic methods use data from somatic tumor gene collections containing or lacking polyploidy genes(PGCC genes)and compare them to genes from evolutionary node taxa.I analyze whether the selected taxa are suitable to resolve the above contradiction or not.Both cancer and amoebae life cycles have a reproductive asexual germline that produces germline stem cells(GSCs)and somatic cell lines that cannot.When the germline loses its reproductive function,the soma-to-germ transition forms a new reproductive germline.The reproductive polyploidy of cancer is homologous to the reproductive polyploidy of unicellular cysts.PGCCs repair DNA defects,reorganize the involved genome architecture and produce new GSCs.The present study refutes the dogma of the early metazoan origin of cancer.Cancer has a unicellular life cycle that was adopted by early metazoans to rescue themselves from evolutionary dead ends.Early metazoans controlled the unicellular life cycle through suppressor and anti-suppressor genes that could suspend or reactivate it.They are the archetypes of tumor suppressor genes and oncogenes.Cells of mammalians and humans that reach a similar impasse as early metazoans can reactivate the conserved life cycle of unicellularians. 展开更多
关键词 Cancer ENTAMOEBA Gene age Life cycle POLYPLOIDY CSCs EMT pgcc
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