[目的]探讨CDCA7L在结肠癌组织中表达及临床意义。[方法]通过QRT-PCR及免疫组织化学法检测CDCA7L m RNA及蛋白在65例结肠癌组织及癌旁组织标本中的表达,分析其表达与患者临床病理特征及预后的关系。[结果]CDCA7L在结肠癌组织标本中的表...[目的]探讨CDCA7L在结肠癌组织中表达及临床意义。[方法]通过QRT-PCR及免疫组织化学法检测CDCA7L m RNA及蛋白在65例结肠癌组织及癌旁组织标本中的表达,分析其表达与患者临床病理特征及预后的关系。[结果]CDCA7L在结肠癌组织标本中的表达较癌旁组织明显增高(81.54%vs 6.15%,P<0.001)。CDCA7L的表达与患者性别、年龄及肿瘤部位无关(P均>0.05),与分期、淋巴结转移、远处转移、肿瘤分化、血清CEA水平及生存状态明显相关(P均<0.05)。高表达CDCA7L患者的总生存时间及中位生存时间均较低表达者明显缩短(27.00±3.32个月vs 43.72±3.08个月,13.00±1.49个月vs 27.01±1.87个月;P<0.001)。Cox多因素回归模型分析提示,CDCA7L表达、远处转移及临床分期是结肠癌独立的预后因素(P<0.05)。[结论]CDCA7L参与调节结肠癌的发生发展,可作为潜在的结肠癌诊断和预后评估的分子标志物。展开更多
Objective Increased expression of CDCA7 is associated with a poorer prognosis in patients with non-small-cell lung cancer(NSCLC).This study was performed to investigate the effects of down-regulating cell division cyc...Objective Increased expression of CDCA7 is associated with a poorer prognosis in patients with non-small-cell lung cancer(NSCLC).This study was performed to investigate the effects of down-regulating cell division cycle-associated 7(CDCA7)gene expression on the proliferation,migration,invasion,cell cycle and apoptosis of human NSCLC cell lines.Methods Cultured A549 and NCI-H292 cells were transfected with si NC(control group)or si CDCA7(experimental group).Cell activity was detected using the CCK-8 and a Real Time Cell Analyzer(RTCA).Cell migration and invasion were also measured by RTCA.In addition,flow cytometry was used to assess the cell cycle progression and apoptosis in the cells,and Western blotting was used to detect the expression level of proteins in key signaling pathways.Results Compared with the cells transfected with si NC,the cell proliferation was significantly reduced(P<0.05),the migration and invasion were decreased,and the cell cycle was blocked in the G0/G1 phase(P<0.05)in the cells transfected with si CDCA7.The number of cells undergoing apoptosis was also increased(P<0.05).Western blotting revealed that P-ERK,Cyclin-D1,Vimentin and Bcl-2 were all downregulated.However,the expression of E-cadherin was not affected by the down-regulation of CDCA7,suggesting that it is upstream of this gene.Conclusion Silencing the CDCA7 gene inhibited the proliferation,migration and invasion of A549 and NCI-H292 cells,hindered the cell cycle transition to the S phase,and promoted cell apoptosis.These findings indicate that CDCA7 may represent a new therapeutic target for NSCLC.展开更多
基金a grant from the National Natural Science Foundation of China(No.81860494 to SY Zheng)。
文摘Objective Increased expression of CDCA7 is associated with a poorer prognosis in patients with non-small-cell lung cancer(NSCLC).This study was performed to investigate the effects of down-regulating cell division cycle-associated 7(CDCA7)gene expression on the proliferation,migration,invasion,cell cycle and apoptosis of human NSCLC cell lines.Methods Cultured A549 and NCI-H292 cells were transfected with si NC(control group)or si CDCA7(experimental group).Cell activity was detected using the CCK-8 and a Real Time Cell Analyzer(RTCA).Cell migration and invasion were also measured by RTCA.In addition,flow cytometry was used to assess the cell cycle progression and apoptosis in the cells,and Western blotting was used to detect the expression level of proteins in key signaling pathways.Results Compared with the cells transfected with si NC,the cell proliferation was significantly reduced(P<0.05),the migration and invasion were decreased,and the cell cycle was blocked in the G0/G1 phase(P<0.05)in the cells transfected with si CDCA7.The number of cells undergoing apoptosis was also increased(P<0.05).Western blotting revealed that P-ERK,Cyclin-D1,Vimentin and Bcl-2 were all downregulated.However,the expression of E-cadherin was not affected by the down-regulation of CDCA7,suggesting that it is upstream of this gene.Conclusion Silencing the CDCA7 gene inhibited the proliferation,migration and invasion of A549 and NCI-H292 cells,hindered the cell cycle transition to the S phase,and promoted cell apoptosis.These findings indicate that CDCA7 may represent a new therapeutic target for NSCLC.
