目的:探索AURKB和TOP2A在乳头状肾细胞癌(PRCC)组织中的表达及与预后的相关性。方法:从TCGA(the cancer genome atlas)数据库下载乳头状肾细胞癌mRNA的表达数据以及乳头状肾细胞癌患者的临床数据,利用R软件的相关包进行差异分析,筛选出...目的:探索AURKB和TOP2A在乳头状肾细胞癌(PRCC)组织中的表达及与预后的相关性。方法:从TCGA(the cancer genome atlas)数据库下载乳头状肾细胞癌mRNA的表达数据以及乳头状肾细胞癌患者的临床数据,利用R软件的相关包进行差异分析,筛选出差异基因。将差异基因导入STRING和Cytoscape中得到差异基因蛋白相互作用网络以及前10个关键基因,并通过GEPIA数据库验证,得到AURKB和TOP2A。进一步绘制出AURKB及TOP2A在PRCC中的表达及与临床预后的关系。最后我们选取部分肾乳头状细胞癌手术石蜡组织标本进行了实验验证。结果:AURKB和TOP2A在乳头状肾细胞癌组织中的表达量较癌旁组织中显著提高,与预后及临床特征有明显相关性,且AURKB与TOP2A表达量越高乳头状肾细胞癌患者预后越差。结论:应用生物信息学方法发现AURKB和TOP2A可能是作为PRCC预后指标。展开更多
[Objectives]To explore the inhibitory effect of AURKB gene in apoptosis and cancer cell growth in HCT 116 cells.[Methods]The in vitro cytology studies were carried out to confirm the expression of the AURKB gene in HC...[Objectives]To explore the inhibitory effect of AURKB gene in apoptosis and cancer cell growth in HCT 116 cells.[Methods]The in vitro cytology studies were carried out to confirm the expression of the AURKB gene in HCT 116 cells and make clear its role in cell activity,cell cycle control and apoptosis,and investigate the effect of AURKB gene in colorectal cancer(CRC).Quantitative reverse transcription/polymerase chain reaction(PCR)analysis and immunofluorescence(IF)staining for markers of AURKB gene were used to examine the effect of AURKB on HCT 116.The AURKB gene target was examined using western blot analysis.In addition,inhibition of AURKB expression was examined using RNA interference(RNAi)on HCT 116 cells in vitro.[Results]HCT 116 cells infected with AURKB shRNA virus suppressed expression of AURKB in vitro.AURKB gene knockdown HCT 116 cells showed reducing cell apoptosis in vitro.Finally,it demonstrated that AURKB function can induce apoptosis of HCT cells.[Conclusions]AURKB is a key regulator of colorectal cancer.AURKs are potential novel molecular targets for the prevention of cancer cell proliferation.展开更多
Aurora kinases have become a hot topic for research as they have been found to play an important role in various stages of mitotic cell division and to participate in malignant conversions of tumors. The participation...Aurora kinases have become a hot topic for research as they have been found to play an important role in various stages of mitotic cell division and to participate in malignant conversions of tumors. The participation of Aurora kinases in the regulation of oocyte meiosis has been recently reported, but their participation in mammalian early embryonic development remained unclear. The object of our study was to establish the spatio-temporal expression pattern of Aurora kinase B (AURKB) in mouse zygotes during the first cleavage, to reveal its functions in the early development of mouse zygotes, and to define the involvement of AURKB in mitogen-activated protein kinase (MAPK) signaling. Our results showed that in mouse zygotes AURKB expression increased in G1 phase and peaked in M phase. AURKB protein distribution was found to be in association with nuclei and distributed throughout the cytoplasm in a cell cycle-dependent manner. Functional disruption of AURKB resulted in abnormal division phenotypes or mitotic impairments. U0126, a specific mitogen-activated protein kinase kinase (MEK) inhibitor, caused significantly altered morphologies of early embryos together with a decrease in protein expression and kinase activity of AURKB. Our results indicated that the activity of AURKB was required for regulating multiple stages of mitotic progression in the early development of mouse zygotes and was correlated with the activation of the MAPK pathway.展开更多
文摘目的:探索AURKB和TOP2A在乳头状肾细胞癌(PRCC)组织中的表达及与预后的相关性。方法:从TCGA(the cancer genome atlas)数据库下载乳头状肾细胞癌mRNA的表达数据以及乳头状肾细胞癌患者的临床数据,利用R软件的相关包进行差异分析,筛选出差异基因。将差异基因导入STRING和Cytoscape中得到差异基因蛋白相互作用网络以及前10个关键基因,并通过GEPIA数据库验证,得到AURKB和TOP2A。进一步绘制出AURKB及TOP2A在PRCC中的表达及与临床预后的关系。最后我们选取部分肾乳头状细胞癌手术石蜡组织标本进行了实验验证。结果:AURKB和TOP2A在乳头状肾细胞癌组织中的表达量较癌旁组织中显著提高,与预后及临床特征有明显相关性,且AURKB与TOP2A表达量越高乳头状肾细胞癌患者预后越差。结论:应用生物信息学方法发现AURKB和TOP2A可能是作为PRCC预后指标。
文摘[Objectives]To explore the inhibitory effect of AURKB gene in apoptosis and cancer cell growth in HCT 116 cells.[Methods]The in vitro cytology studies were carried out to confirm the expression of the AURKB gene in HCT 116 cells and make clear its role in cell activity,cell cycle control and apoptosis,and investigate the effect of AURKB gene in colorectal cancer(CRC).Quantitative reverse transcription/polymerase chain reaction(PCR)analysis and immunofluorescence(IF)staining for markers of AURKB gene were used to examine the effect of AURKB on HCT 116.The AURKB gene target was examined using western blot analysis.In addition,inhibition of AURKB expression was examined using RNA interference(RNAi)on HCT 116 cells in vitro.[Results]HCT 116 cells infected with AURKB shRNA virus suppressed expression of AURKB in vitro.AURKB gene knockdown HCT 116 cells showed reducing cell apoptosis in vitro.Finally,it demonstrated that AURKB function can induce apoptosis of HCT cells.[Conclusions]AURKB is a key regulator of colorectal cancer.AURKs are potential novel molecular targets for the prevention of cancer cell proliferation.
基金supported by the National Natural Science Foundation of China (Grant No. 81070527)
文摘Aurora kinases have become a hot topic for research as they have been found to play an important role in various stages of mitotic cell division and to participate in malignant conversions of tumors. The participation of Aurora kinases in the regulation of oocyte meiosis has been recently reported, but their participation in mammalian early embryonic development remained unclear. The object of our study was to establish the spatio-temporal expression pattern of Aurora kinase B (AURKB) in mouse zygotes during the first cleavage, to reveal its functions in the early development of mouse zygotes, and to define the involvement of AURKB in mitogen-activated protein kinase (MAPK) signaling. Our results showed that in mouse zygotes AURKB expression increased in G1 phase and peaked in M phase. AURKB protein distribution was found to be in association with nuclei and distributed throughout the cytoplasm in a cell cycle-dependent manner. Functional disruption of AURKB resulted in abnormal division phenotypes or mitotic impairments. U0126, a specific mitogen-activated protein kinase kinase (MEK) inhibitor, caused significantly altered morphologies of early embryos together with a decrease in protein expression and kinase activity of AURKB. Our results indicated that the activity of AURKB was required for regulating multiple stages of mitotic progression in the early development of mouse zygotes and was correlated with the activation of the MAPK pathway.
