细胞周期蛋白质类
细胞周期蛋白质类的相关文献在2001年到2022年内共计67篇,主要集中在肿瘤学、基础医学、妇产科学
等领域,其中期刊论文67篇、专利文献320201篇;相关期刊47种,包括中国实验诊断学、中华检验医学杂志、中华肝脏病杂志等;
细胞周期蛋白质类的相关文献由316位作者贡献,包括何松、刘丹丹、漆洪波等。
细胞周期蛋白质类—发文量
专利文献>
论文:320201篇
占比:99.98%
总计:320268篇
细胞周期蛋白质类
-研究学者
- 何松
- 刘丹丹
- 漆洪波
- 罗欣
- Chen Bo
- Han Conghui
- Hao Lin
- Li Meili
- Pang Kun
- Shi Zhenduo
- Zang Guanghui
- Zhou Rongsheng
- 万自芬
- 严丽华
- 严睿成
- 于洁
- 付家欣
- 付莛凯
- 任智星
- 任静(综述)
- 何小玲
- 何常
- 何建昌
- 余家俊
- 余红
- 余艳红
- 侯兰芬
- 侯波
- 俞松
- 俞翬
- 傅博
- 党苗苗
- 兰伟途
- 兰文达
- 关明
- 冯新莉
- 冯艳铭
- 刘伏友
- 刘军
- 刘刚
- 刘子杰
- 刘彦琴
- 刘晓菊
- 刘景华
- 刘楠
- 刘海鸥
- 刘维薇
- 刘艳杰
- 包海荣
- 卓莉
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任智星;
杨光华
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摘要:
目的 探讨细胞分裂周期相关蛋白 8(CDCA8)在前列腺癌(PCa)中的表达及作用机制。方法 通过生物 信息学方法分析正常前列腺组织和 PCa组织中 CDCA8 mRNA水平差异。利用癌症基因组图谱(TCGA)数据库中 RNA表达测序数据分析 CDCA8表达相关的 PCa患者无病生存期(DFS)。免疫组织化学方法检测根治性前列腺切除 术后 56例 PCa组织和癌旁组织中 CDCA8蛋白表达差异,并依据染色指数将 PCa患者分为 CDCA8蛋白高表达组(31 例)和低表达组(25例),分析患者临床特征与 CDCA8表达水平的相关性。利用 siRNA沉默 PCa细胞 CDCA8基因,实 时荧光定量聚合酶链反应(qPCR)检测 CDCA8 mRNA的表达水平,细胞克隆形成实验检测 PCa细胞增殖能力,蛋白 免疫印迹法检测 CDCA8、Ki67、增殖细胞核抗原(PCNA)以及磷脂酰肌醇-3-激酶(PI3K)/蛋白激酶 B(AKT)信号通路 蛋白表达的变化。结果 TCGA数据库中 PCa组织中 CDCA8 mRNA水平明显高于正常组织,CDCA8 mRNA高表达的 患者预后更差(P<0.01)。PCa组织 CDCA8的蛋白表达水平明显高于癌旁组织,且表达水平与患者总前列腺特异性 抗原(tPSA)、Gleason评分、T分期和术后切缘情况呈正相关(P<0.01)。CDCA8蛋白高表达组tPSA≥10 μg/L、T3期、术 后切缘阳性患者比例大于 CDCA8 蛋白低表达组(P<0.05)。沉默 CDCA8 基因后 PCa 细胞增殖能力减弱,Ki67、 PCNA、p-PI3K、p-AKT蛋白表达水平均下调(P<0.01)。结论 CDCA8通过调控增殖促进 PCa发生,其作用机制可 能与 PI3K/AKT信号通路有关。
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兰伟途;
武峰;
何建昌;
兰文达;
王万宏
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摘要:
目的 探讨miR-199a-5p靶向细胞分裂周期相关7样蛋白(CDCA7L)对胶质瘤细胞迁移及侵袭的影响.方法 采用实时荧光定量PCR(RT-qPCR)检测人正常星形胶质细胞HA1800与人胶质瘤细胞株U251中miR-199a-5p表达量;使用Lipofectamine 2000转染试剂盒对U251细胞进行转染,并分别命名为空白组(正常培养的U251细胞)、miR-NC组(转染miR-?NC)、miR-199a-5p mimic组(转染miR-199a-5p mimic)、miR-199a-5p?mimic+pcDNA组(共转染miR-199a-5p mimic和pcDNA)、miR-199a-5p?mimic+pcDNA-CDCA7L组(共转染miR-199a-5p mimic和pcDNA-CDCA7L),Transwell实验检测U251细胞迁移、侵袭能力,Western blot检测CDCA7L蛋白表达情况;利用TargetScan软件预测miR-199a-5p和CDCA7L结合位点;双荧光素酶报告基因检测验证miR-199a-5p与CDCA7L靶向关系;HA1800、U251两组细胞间的比较采用两样本t检验;多组间比较采用单因素方差分析,两组间比较采用SNK-q检验.结果 与HA1800细胞比较,U251细胞中miR-199a-5p表达水平降低(1.09±0.26比0.32±0.14),CDCA7L蛋白表达量升高(0.21±0.02比0.85±0.13),差异具有统计学意义(P均<0.001).miR-199a-5p mimic组细胞迁移数、侵袭数及CDCA7L蛋白表达量均低于空白组、miR-?NC组(50.12±3.36比94.57±7.14、93.86±6.11;42.53±3.34比71.49±4.35、73.76±4.21;0.25±0.07比0.83±0.12、0.89±0.09),差异具有统计学意义(P均<0.001).CDCA7L为miR-199a-5p靶基因.过表达CDCA7L可逆转miR-199a-5p对U251细胞迁移及侵袭的抑制作用(P<0.05).结论 在胶质瘤细胞中miR-199a-5p呈低表达,上调miR-199a-5p可能通过靶向抑制CDCA7L蛋白表达,进而抑制胶质瘤细胞的迁移和侵袭.
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Pang Kun;
Li Meili;
Chen Bo;
Hao Lin;
Shi Zhenduo;
Zhou Rongsheng;
Zang Guanghui;
Han Conghui
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摘要:
目的 研究基本同源物增强子(ERH)对人膀胱癌T24和5637细胞迁移和侵袭作用的影响.方法 将人膀胱癌T24和5637细胞的ERH敲除后,采用细胞划痕实验、Transwell细胞迁移实验、Transwell细胞侵袭实验验证其迁移和侵袭功能变化,Western blot检测细胞迁移与侵袭相关蛋白的表达,并通过裸鼠尾静脉转移实验验证敲除ERH基因后在体内对膀胱癌细胞转移能力的影响.结果 (1)细胞划痕实验结果显示,敲除ERH基因后的人膀胱癌5637和T24细胞迁移率均明显降低(P<0.05);(2)Transwell细胞迁移实验、Transwell细胞侵袭实验结果显示,敲除ERH基因后的人膀胱癌5637和T24细胞迁移细胞计数和侵袭细胞计数均明显减少(P<0.05).(3)Western blot实验结果显示,敲除ERH基因后的人膀胱癌5637细胞和T24细胞中E-Cadherin表达明显升高(P<0.05),而Fibronectin、Twist、Vimentin、Snail2蛋白的表达明显降低(P<0.05).(4)裸鼠尾静脉转移实验显示,与ERH正常组相比,ERH敲除组小鼠肺转移灶明显减少.结论 体外和体内实验均提示,ERH基因敲除影响人膀胱癌T24和5637细胞的迁移与侵袭.%Objective To study the effect of enhancer of rudimentary homolog (ERH) gene on migration and invasion in human bladder cancer T24 and 5637 cells.Methods After knocking out the ERH gene of human bladder cancer T24 and 5637 cells,Wound healing assay,Transwell cell migration assay and Transwell cell invasion assay were used to verify the migration and invasion function.Cell migration related protein was detected by Western blot.Nude mouse tail vein transfer assay was used to study the metastasis ability of bladder cancer cells in vivo.Results (1) The Wound healing assay showed that there were significant differences in the migration cell counts of human bladder cancer 5637 and T24 (P < 0.05).(2) There were significant differences in migration and invasion cell counts of Transwell assay (P <0.05).(3) Western blot showed that the expression of E-Cadherin in human bladder cancer 5637 cells and T24 cells was significantly increased (P < 0.05) after knocking out ERH gene,while the expression of Fibronectin,Twist,Vimentin and Snail2 protein were significantly decreased (P < 0.05).(4) Nude mouse tail vein transfer assay showed that lung metastases were significantly reduced in the ERH knockout group compared with the normal ERH group.Conclusions Both in vitro and in vivo experiments suggest that ERH knockout affects the migration and invasion of human bladder cancer T24 and 5637 cells.
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慈延东1;
邱晨生1;
吴晓淋1;
方晓露1;
相宏飞1;
陈伯华1
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摘要:
目的比较细胞周期D1型结合蛋白1(CCNDBP1)在不同年龄阶段腰椎间盘突出症病人椎间盘中的表达,探讨其与腰椎间盘退变的关系。方法收集不同年龄阶段腰椎间盘突出症病人共42例,其中30~岁、40~岁、50~岁年龄段病人各14例。取病人突出的椎间盘组织,苏木精-伊红染色观察其退变情况,采用免疫组化法、PCR法、Western印迹法从细胞、基因、蛋白水平检测CCNDBP1的表达量。结果苏木精-伊红染色结果显示,各个年龄阶段腰椎间盘突出症病人腰椎间盘组织均有不同程度退变,退变程度与年龄呈正相关。免疫组化法、PCR法和Western印迹法检测结果显示,腰椎间盘组织CCNDBP1的表达随病人年龄的增加而减少,其中30~岁年龄段病人CCNDBP1的表达显著高于40~岁年龄段病人,差异有统计学意义(F=15.42~168.30,t=3.06~6.78,P<0.05),40~岁年龄段病人CCNDBP1的表达显著高于50~岁年龄段病人,差异有统计学意义(t=2.58~9.91,P<0.05)。结论人腰椎间盘髓核组织退变过程中有CCNDBP1的参与,随着年龄的增长,CCNDBP1在退变腰椎间盘组织中的表达量逐渐减少。
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王勇;
郭永连;
陈琳;
李国灏;
余家俊;
程薇
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摘要:
目的 探讨微小RNA-1180(miR-1180)转染对肾癌细胞系786-O和ACHN生长的影响.方法 肾癌细胞分为两组:dsControl组和miR-1180组.实时定量(qRT)-PCR检测p21 mRNA的表达变化.Western blot检测p21、细胞周期蛋白依赖性激酶(CDK)4、CDK6和CyclinD1蛋白的表达变化.流式细胞术(FCM)检测细胞周期变化,使用多靶扫描法(MTS)和集落形成实验检测细胞活力和增殖能力.结果 qRT-PCR结果显示,与对照组相比,转染miR-1180后786-O和ACHN细胞中p21 mR-NA水平分别上调2.54倍(P<0.01)和2.49倍(P<0.01).p21蛋白表达趋势与qRT-PCR结果相符,CDK4、CDK6和CyclinD1蛋白的表达明显下调.FCM结果显示,转染miR-1180后,位于G0/G1期的细胞比例明显增大,而位于S期和G2/M期的细胞比例明显下降,表明细胞周期被阻滞在Go/G1期.MTS结果显示,与dsControl组相比,转染miR-1180后,两种肾癌细胞活力明显降低.集落形成实验显示,miR-1180组的集落数数量明显较少,表明细胞增殖能力降低.结论 miR-1180能显著激活肾癌细胞中p21蛋白的表达,并抑制肾癌细胞786-O和ACHN的生长.%Objective To investigate the effect of microRNA-1180 transfection on the growth of renal cell carcinoma lines 786-O and ACHN.Methods The renal carcinoma cells were divided into the two groups:control group (transfecting dsControl) and experimental group (transfecting miR-1180).The expression change of p21 mRNA was detected by qRT-PCR.Western blot was conducted to analyze the expression changes of p21,CDK4,CDK6 and CyclinD1 proteins.Flow cytometry (FCM) was used to detect the cell cycle change.The MTS assay was conducted to detect the cell viability and the colony forming assay was performed to examine the cell proliferation ability.Results The qRT-PCR results showed that compared with the negative control dsControl group,after miR-1180 transfection,the expression level of·p21 mRNA in 786-O and ACHN cells was up-regulated to 2.54-fold and 2.49-fold respectively(P<0.01).The expression trend of p21 protein was consistent with qRT-PCR results.The expression of CDK4,CDK6 and CyclinD1 proteins were significantly down-regulated.The FCM results showed that the proportion of cells in G0/ G1 phase was significantly increased after transfection of miR-1180,but the proportion of cells in S phase and G2/M phase was decreased significantly,indicating that the cell cycle was arrested in G0/G1 phase.The MTS assay results showed that compared with the dsControl group,the viability of the two kinds of renal carcinoma cells was significantly decreased.The colony formation assay showed that the number of colonies formed in the miR-1180 group was smaller,indicating the proliferation ability of miR-1180 transfected cells was decreased.Conclusion miR-1180 can significantly activate the p21 protein expression and inhibit the growth of renal carcinoma cell lines 786-O and ACHN.
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陈婧;
张克难;
王宽宇;
赵征
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摘要:
目的 分析细胞分裂周期相关7样蛋白(CDCA7L)在脑胶质瘤患者中的表达情况、临床意义和可能参与的生物学过程,并通过实验初步验证该蛋白在脑胶质瘤中的功能.方法 回顾性纳入中国脑胶质瘤基因组图谱计划(CGGA) mRNA芯片数据库中309例脑胶质瘤患者的临床资料及mRNA芯片数据,分析CDCA7L蛋白的表达特征.同时以TCGA RNA测序数据库中的胶质瘤数据作为独立验证数据集,采用t检验、方差分析和秩和检验分析CDCA7L基因的表达特征.利用Kaplan-Meier生存曲线和Log-rank检验评价CDCA7L蛋白对胶质瘤患者预后的作用.通过基因本体分析获得CDCA7L蛋白相关基因的功能和可能参与的信号通路.采用Transwell小室检测敲低CDCA7L蛋白表达对胶质瘤细胞株垂直迁移的影响.应用流式细胞术检测敲低CDCA7L蛋白对胶质瘤细胞株凋亡的作用.结果 在世界卫生组织(WHO)Ⅱ、Ⅲ和Ⅳ级脑胶质瘤中,CDCA7L的表达量随着病理级别的增加而逐渐升高[分别为0.053(0.051)、0.083(0.078)和0.133(0.152),均P<0.05];CDCA7L在异柠檬酸脱氢酶(IDH)野生型脑胶质瘤中的表达水平高于突变型[分别为0.123(0.165)和0.068(0.068),P<0.001].在胶质瘤中CDCA7L蛋白高表达组患者的累积生存率明显低于低表达组(P<0.001).在胶质瘤细胞株中敲低CDCA7L抑制细胞的垂直迁移,增加了凋亡细胞的百分比(均P<0.01).结论 CDCA7L蛋白可能与胶质瘤细胞的细胞周期、细胞分裂、DNA复制、DNA损伤修复和染色体分离等生物学过程和信号通路有关.CDCA7L蛋白可促进脑胶质瘤的发展和肿瘤细胞的迁移,抑制肿瘤细胞的凋亡,可作为患者预后判断的指标及潜在的治疗靶点.%Objectives To analyze the expression and function of cell division cycle-associated 7-like protein (CDCA7L) in gliomas and to investigate the biological processes and signal pathway involved in glioma cells by CDCA7L.Methods The clinical data and CDCA7L expression information of 309 glioma patients were collected retrospectively from the CGGA mRNA sequencing data.TCGA mRNA sequencing was used as validation sets.Kaplan-Meier method and log-rank test were used to estimate the role of CDCA7L in the prognosis of patients.Gene ontology (GO) and KEGG pathway analysis were used to obtain biological processes and signal pathway involved in CDCA7L expression.Transwell chamber assay was used to detect the effect of knockdown of CDCA7L protein on migration of glioma cell lines.Flow cytometry was used to analyze the effect of knockdown of CDCA7L protein on glioma cell line apoptosis.Results CDCA7L was significantly upregulated along with tumor grades progress of glioma [0.053 (0.051),0.083 (0.078) and 0.133 (0.152),respectively from WHO Ⅱ to Ⅳ,all P <0.05].The expression of CDCA7L was higher in IDH wild-type gliomas [0.123 (0.165)and 0.068 (0.068),P < 0.001].Survival analysis revealed that high expression of CDCA7L indicated a poor survival outcome (P < 0.001).Knockdown of CDCA7L inhibited glioma cell migration and promoted apoptotic (all P < 0.01).Conclusions CDCA7L may be associated with the biological processes and signal pathway of glioma such as cell cycle,cell division,DNA replication,DNA repair and chromosome segregation.CDCA7L could promote the development of glioma and thus be used as a prognostic indicator and a potential therapeutic target.
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潘亚琼1;
戴忠1;
左长清1;
汪宗桂2
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摘要:
背景:最近研究发现,长链非编码RNA可调控干细胞的增殖与分化,但关于长链非编码RNA NR_033474在干细胞增殖及细胞周期调控中的作用,目前尚不清楚。目的:通过在C3H10T1/2间质干细胞中过表达NR_033474,观察NR_033474对C3H10T1/2细胞增殖和细胞周期的影响,进一步分析NR_033474影响间质干细胞C3H10T1/2增殖的可能作用机制。方法:通过慢病毒载体在C3H10T1/2细胞中过表达NR_033474,应用Real-time PCR检测其表达效率,以转染空载体慢病毒的C3H10T1/2细胞为对照,利用细胞计数法绘制生长曲线,观察过表达NR_033474后C3H10T1/2细胞的生长变化;PI染色流式细胞仪检测细胞周期改变;通过Western蛋白印迹法检测过表达NR_033474后,细胞周期相关蛋白(P53、Cyclin B1、CDK1、Cyclin D1)的表达。结果与结论:(1)与对照组比较,感染NR_033474慢病毒后的C3H10T1/2间质干细胞NR_033474表达上调约100倍(P〈0.01);(2)与对照组比较,过表达NR_033474后的C3H10T1/2细胞增殖能力明显降低(P〈0.05);(3)与对照组比较,过表达NR_033474后的C3H10T1/2间质干细胞阻滞于G2/M期;(4)与对照组比较,过表达NR_033474后的C3H10T1/2间质干细胞Cyclin B1和CDK1蛋白表达下调,P53、Cyclin D1蛋白水平无明显变化;(5)结果表明,NR_033474可能通过下调Cyclin B1及CDK1蛋白表达水平,抑制C3H10T1/2间质干细胞的增殖生长能力,使细胞阻滞于G_2/M期。
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张桂东
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摘要:
目的探讨细胞周期蛋白D1(CyclinD1)和细胞分裂周期蛋白25A(CDC25A)mRNA在胆囊癌组织中的表达及其临床意义。方法采用逆转录-聚合酶链式反应方法测定44例胆囊癌以及35例慢性胆囊炎黏膜组织中CyclinD1、CDC25A mRNA的表达水平。结果胆囊癌组织中CyclinD1、CDC25A mRNA表达量与慢性胆囊炎黏膜组织比较,差异均有显著性(t=5.84、11.44,P<0.05);但胆囊癌组织中CyclinD1、CDC25A mRNA表达量与淋巴结转移无关。结论 CyclinD1、CDC25A mRNA的表达与胆囊癌的发病有关,但与病人预后无关。