目的 研究核仁纺锤体相关蛋白1 (Nucleolar and spindle associated protein 1,NUSAP1)在胰腺癌组织中的表达及临床预后分析。方法 利用GEPIA数据库检索NUSAP1基因在胰腺癌组织和正常组织中的表达水平,TCGA数据库及组织芯片研究及验证NU...目的 研究核仁纺锤体相关蛋白1 (Nucleolar and spindle associated protein 1,NUSAP1)在胰腺癌组织中的表达及临床预后分析。方法 利用GEPIA数据库检索NUSAP1基因在胰腺癌组织和正常组织中的表达水平,TCGA数据库及组织芯片研究及验证NUSAP1在胰腺癌的临床预后分析。结果 GEPIA数据库分析结果显示胰腺癌组织中NUSAP1的表达高于正常对照组(P<0.05)。TCGA数据库结果显示,高表达NUSAP1的胰腺癌患者生存时间较低表达NUSAP1的患者更短(HR=2.02,P<0.05)。在病理分级G3-G4组、残余瘤R1和R2组、胰腺癌治疗进展组中NUSAP1的表达均分别高于病理分级G1-G2组、残余瘤R0组、治疗缓解组(P<0.05)。在死亡组中,NUSAP1的表达高于存活组(P<0.05)。组织芯片免疫组化结果显示,与癌旁组织相比,NUSAP1在胰腺癌中呈高表达(χ^(2)=44.10,P<0.001),NUSAP1高表达的患者生存时间更短,预后越差。单因素回归分析结果显示NUSAP1的表达量、性别、病理分级、肿瘤大小、T分期、N分期、TNM分期是影响胰腺癌患者总生存期的危险因素(P<0.05)。多因素回归分析结果显示NUSAP1的表达量、TNM分期是影响总生存期的独立危险因素(P<0.05)。结论 NUSAP1在胰腺癌组织中高表达,与胰腺癌患者不良预后相关。展开更多
目的:探讨核仁纺锤体相关蛋白1(nucleolar and spindle-associated protein 1,NUSAP1)在食管癌(esophageal carci⁃noma,ESCA)中的表达情况、临床意义及功能机制,为ESCA的早期诊断和治疗提供新思路。方法:从GEPIA2和TIMER数据库下载ESCA...目的:探讨核仁纺锤体相关蛋白1(nucleolar and spindle-associated protein 1,NUSAP1)在食管癌(esophageal carci⁃noma,ESCA)中的表达情况、临床意义及功能机制,为ESCA的早期诊断和治疗提供新思路。方法:从GEPIA2和TIMER数据库下载ESCA样本与癌旁样本,进行NUSAP1的表达分析,STRING和Cytoscape软件进行NUSAP1相关基因的PPI网络构建,并进行GO、KEGG及GSEA富集分析。TIMER数据库被用来分析NUSAP1与免疫细胞的相关性。最后通过RT-PCR、Western blot和免疫组化验证NUSAP1在ESCA组织和细胞中的表达,使用慢病毒包被的小干扰RNA转染ESCA细胞,进行NUSAP1的表达敲减。通过CKK-8和Ki67免疫荧光评估NUSAP1对ESCA细胞增殖的影响。结果:NUSAP1在ESCA组织和细胞中高表达。NUSAP1的表达与CDK1、B细胞和巨噬细胞浸润正相关,而与CD4+T细胞、CD8+T细胞、中性粒细胞和树突状细胞浸润负相关。GSEA分析发现NUSAP1的高表达组主要富集于Wnt/β-catenin信号通路、过氧化物酶通路、PI3K/Akt/mTOR信号通路。在体外,敲减NUSAP1后抑制了ESCA细胞增殖。结论:NUSAP1在ESCA中高表达,并与ESCA细胞增殖和免疫细胞浸润密切相关。因此,NUSAP1可能有助于ESCA的诊断和治疗。展开更多
核仁G蛋白1(Nucleolar G protein 1,NOG1)是一种高度保守的核仁GTP酶,在真核生物中广泛存在,参与60 S核糖体亚基前体的组装。在线虫中敲减NOG1的表达造成生长缓慢、虫体变小和寿命延长的表型,而过量表达NOG1则使线虫的寿命缩短。拟南芥...核仁G蛋白1(Nucleolar G protein 1,NOG1)是一种高度保守的核仁GTP酶,在真核生物中广泛存在,参与60 S核糖体亚基前体的组装。在线虫中敲减NOG1的表达造成生长缓慢、虫体变小和寿命延长的表型,而过量表达NOG1则使线虫的寿命缩短。拟南芥的At1g10300基因注释为NOG1-2,但是其生物学功能还有待研究。该研究对其功能进行了初步研究,首先检测了该基因在拟南芥各个器官的表达情况。结果表明:该基因在7 d龄幼苗、茎生叶和花中均有表达,其中在花中表达量最高。获得了At1g10300基因的T-DNA插入突变体,发现在长日照条件下,At1g10300突变体植株的莲座紧凑,莲座叶片长宽比降低,但叶面积和植株高度与野生型相比无显著差异,表明其叶形发生改变;突变体植株的抽薹时间晚于野生型。荧光定量RT-PCR结果表明,突变体植株中开花促进因子FT、CO和GI的表达水平下调,而开花抑制因子FLC的表达水平上调。以上结果揭示At1g10300基因的突变影响了FT、CO、GI及FLC基因的表达,使植株出现晚花表型。展开更多
目的探讨核仁纺锤体相关蛋白1(nucleolar spindle-associated protein 1,NuSAP1)在宫颈癌组织中的表达与临床病理特征的关系及其临床意义。方法采用Envision二步法免疫组织化学染色检测NuSAP1蛋白在宫颈癌及正常宫颈组织中的表达情况,...目的探讨核仁纺锤体相关蛋白1(nucleolar spindle-associated protein 1,NuSAP1)在宫颈癌组织中的表达与临床病理特征的关系及其临床意义。方法采用Envision二步法免疫组织化学染色检测NuSAP1蛋白在宫颈癌及正常宫颈组织中的表达情况,应用基因公共数据库在线分析NuSAP1 mRNA在宫颈癌和正常宫颈组织中的表达水平。结果NuSAP1蛋白在宫颈癌组织中的高表达率为54.1%(60/111),正常宫颈组织中的高表达率为5.0%(2/40);NuSAP1 mRNA在宫颈癌组织中表达水平高于正常宫颈组织。宫颈癌中NuSAP1蛋白的表达水平与组织分化程度、淋巴结转移、淋巴脉管间隙浸润、间质浸润深度、FIGO分期相关,与患者年龄、肿瘤大小、组织学类型、宫旁浸润无关。NuSAPl蛋白高表达患者的术后复发、转移率高于低表达患者。结论NuSAP1在宫颈癌组织中存在高表达,其表达水平对宫颈癌患者术后复发、转移的预测具有指导意义。展开更多
Objective:Gastric cancer(GC)is a globally common cancer characterized by high incidence and mortality worldwide.Advances in the molecular understanding of GC provide promising targets for GC diagnosis and therapy.Long...Objective:Gastric cancer(GC)is a globally common cancer characterized by high incidence and mortality worldwide.Advances in the molecular understanding of GC provide promising targets for GC diagnosis and therapy.Long non-coding RNAs(lncRNAs)and their downstream regulators are regarded to be implicated in the progression of multiple types of malignancies.Studies have shown that the lncRNA small nucleolar RNA host gene 4(SNHG4)serves as a tumor promoter in various malignancies,while its function in GC has yet to be characterized.Therefore,our study aimed to explore the role and underlying mechanism of SNHG4 in GC.Methods:We used qRT-PCR to analyze SNHG4 expression in GC tissues and cells.Kaplan-Meier analysis was used to assess the correlation between SNHG4 expression and the survival rate of GC patients.Cellular function experiments such as CCK-8,BrdU,colony formation,flow cytometry analysis,and transwell were performed to explore the effects of SNHG4 on GC cell proliferation,apoptosis,cell cycle,migration,and invasion.We also established xenograft mouse models to explore the effect of SNHG4 on GC tumor growth.Mechanically,dual luciferase reporter assay was used to verify the interaction between SNHG4 and miR-409-3p and between miR-409-3p and cAMP responsive element binding protein 1(CREB1).Results:The results indicated that SNHG4 was overexpressed in GC tissues and cell lines,and was linked with poor survival rate of GC patients.SNHG4 promoted GC cell proliferation,migration,and invasion while inhibiting cell apoptosis and cell cycle arrest in vitro.The in vivo experiment indicated that SNHG4 facilitated GC tumor growth.Furthermore,SNHG4 was demonstrated to bind to miR-409-3p.Moreover,CREB1 was directly targeted by miR-409-3p.Rescue assays demonstrated that miR-409-3p deficiency reversed the suppressive impact of SNHG4 knockdown on GC cell malignancy.Additionally,miR-409-3p was also revealed to inhibit GC cell proliferation,migration,and invasion by targeting CREB1.Conclusion:In conclusion,we verified that the SNHG4 promoted GC growth and metastasis by binding to miR-409-3p to upregulate CREB1,which may deepen the understanding of the underlying mechanism in GC development.展开更多
文摘目的:探讨核仁纺锤体相关蛋白1(nucleolar and spindle-associated protein 1,NUSAP1)在食管癌(esophageal carci⁃noma,ESCA)中的表达情况、临床意义及功能机制,为ESCA的早期诊断和治疗提供新思路。方法:从GEPIA2和TIMER数据库下载ESCA样本与癌旁样本,进行NUSAP1的表达分析,STRING和Cytoscape软件进行NUSAP1相关基因的PPI网络构建,并进行GO、KEGG及GSEA富集分析。TIMER数据库被用来分析NUSAP1与免疫细胞的相关性。最后通过RT-PCR、Western blot和免疫组化验证NUSAP1在ESCA组织和细胞中的表达,使用慢病毒包被的小干扰RNA转染ESCA细胞,进行NUSAP1的表达敲减。通过CKK-8和Ki67免疫荧光评估NUSAP1对ESCA细胞增殖的影响。结果:NUSAP1在ESCA组织和细胞中高表达。NUSAP1的表达与CDK1、B细胞和巨噬细胞浸润正相关,而与CD4+T细胞、CD8+T细胞、中性粒细胞和树突状细胞浸润负相关。GSEA分析发现NUSAP1的高表达组主要富集于Wnt/β-catenin信号通路、过氧化物酶通路、PI3K/Akt/mTOR信号通路。在体外,敲减NUSAP1后抑制了ESCA细胞增殖。结论:NUSAP1在ESCA中高表达,并与ESCA细胞增殖和免疫细胞浸润密切相关。因此,NUSAP1可能有助于ESCA的诊断和治疗。
文摘核仁G蛋白1(Nucleolar G protein 1,NOG1)是一种高度保守的核仁GTP酶,在真核生物中广泛存在,参与60 S核糖体亚基前体的组装。在线虫中敲减NOG1的表达造成生长缓慢、虫体变小和寿命延长的表型,而过量表达NOG1则使线虫的寿命缩短。拟南芥的At1g10300基因注释为NOG1-2,但是其生物学功能还有待研究。该研究对其功能进行了初步研究,首先检测了该基因在拟南芥各个器官的表达情况。结果表明:该基因在7 d龄幼苗、茎生叶和花中均有表达,其中在花中表达量最高。获得了At1g10300基因的T-DNA插入突变体,发现在长日照条件下,At1g10300突变体植株的莲座紧凑,莲座叶片长宽比降低,但叶面积和植株高度与野生型相比无显著差异,表明其叶形发生改变;突变体植株的抽薹时间晚于野生型。荧光定量RT-PCR结果表明,突变体植株中开花促进因子FT、CO和GI的表达水平下调,而开花抑制因子FLC的表达水平上调。以上结果揭示At1g10300基因的突变影响了FT、CO、GI及FLC基因的表达,使植株出现晚花表型。
文摘Objective:Gastric cancer(GC)is a globally common cancer characterized by high incidence and mortality worldwide.Advances in the molecular understanding of GC provide promising targets for GC diagnosis and therapy.Long non-coding RNAs(lncRNAs)and their downstream regulators are regarded to be implicated in the progression of multiple types of malignancies.Studies have shown that the lncRNA small nucleolar RNA host gene 4(SNHG4)serves as a tumor promoter in various malignancies,while its function in GC has yet to be characterized.Therefore,our study aimed to explore the role and underlying mechanism of SNHG4 in GC.Methods:We used qRT-PCR to analyze SNHG4 expression in GC tissues and cells.Kaplan-Meier analysis was used to assess the correlation between SNHG4 expression and the survival rate of GC patients.Cellular function experiments such as CCK-8,BrdU,colony formation,flow cytometry analysis,and transwell were performed to explore the effects of SNHG4 on GC cell proliferation,apoptosis,cell cycle,migration,and invasion.We also established xenograft mouse models to explore the effect of SNHG4 on GC tumor growth.Mechanically,dual luciferase reporter assay was used to verify the interaction between SNHG4 and miR-409-3p and between miR-409-3p and cAMP responsive element binding protein 1(CREB1).Results:The results indicated that SNHG4 was overexpressed in GC tissues and cell lines,and was linked with poor survival rate of GC patients.SNHG4 promoted GC cell proliferation,migration,and invasion while inhibiting cell apoptosis and cell cycle arrest in vitro.The in vivo experiment indicated that SNHG4 facilitated GC tumor growth.Furthermore,SNHG4 was demonstrated to bind to miR-409-3p.Moreover,CREB1 was directly targeted by miR-409-3p.Rescue assays demonstrated that miR-409-3p deficiency reversed the suppressive impact of SNHG4 knockdown on GC cell malignancy.Additionally,miR-409-3p was also revealed to inhibit GC cell proliferation,migration,and invasion by targeting CREB1.Conclusion:In conclusion,we verified that the SNHG4 promoted GC growth and metastasis by binding to miR-409-3p to upregulate CREB1,which may deepen the understanding of the underlying mechanism in GC development.
