Objective:Anillin(ANLN)is considered an oncogene in various cancers,but its effect on cervical cancer remains poorly understood.Hence,this study aimed to describe the action of ANLN on cervical cancer development and ...Objective:Anillin(ANLN)is considered an oncogene in various cancers,but its effect on cervical cancer remains poorly understood.Hence,this study aimed to describe the action of ANLN on cervical cancer development and investigate the potential mechanism.Methods:Analysis of ANLN expression and its association with survival in carcinoma and endocervical adenocarcinoma(CESC)patients based on GEO and UALCAN databases.The tumor and adjacent normal tissues of 100 cervical cancer cases were harvested to detect the ANLN expression and explore its relationship with patient survival.Cell proliferation,apoptosis,migration,and invasion were measured by utilizing 5-ethynyl-2′-deoxyuridine(EdU)staining,Flow cytometry,and Transwell assay,respectively.ANLN andWnt expression were analyzed by RT-qPCR andWestern Blot.Results:ANLN was significantly elevated in tumor tissues,and cervical cancer cases with high ANLN expression exhibited poor survival and high dead proportion.Besides,ANLN induced cervical cancer cell proliferation,migration,and invasion and restrained cell apoptosis.In addition,ANLN promoted Wnt/β-catenin pathway activation.Furthermore,ANLN accelerated cell aggressive behaviors and suppressed cell apoptosis via activating the Wnt/β-catenin signaling in cervical cancer.Conclusion:ANLN was enhanced in cervical cancer tissues and related to poor prognosis.ANLN accelerated cervical cancer cell aggressive behaviors and suppressed cell apoptosis via activating theWnt/β-catenin pathway.展开更多
目的研究肌动蛋白结合蛋白(ANLN)、细胞色素P450(Cytochromes P 450,CYPs)亚家族成员CYP2C9、透明质酸介导运动因子受体(HMMR)在乙型肝炎病毒相关肝细胞癌(HBV-HCC)组织中的表达及对其预后的影响。方法收集手术切除的25份HCC标本。采用...目的研究肌动蛋白结合蛋白(ANLN)、细胞色素P450(Cytochromes P 450,CYPs)亚家族成员CYP2C9、透明质酸介导运动因子受体(HMMR)在乙型肝炎病毒相关肝细胞癌(HBV-HCC)组织中的表达及对其预后的影响。方法收集手术切除的25份HCC标本。采用免疫组织化学方法分析ANLN、CYP2C9、HMMR蛋白表达水平在癌组织及癌旁组织的差别,采用Log-Rank检验评估三者对HCC患者术后复发及远期存活的影响。结果HCC患者癌组织的ANLN、CYP2C9免疫反应性评分(IRS)低于癌旁组织分别为(2.4±2.5)分比(3.7±2.7)分(t=2.18,P=0.039)和(4.2±2.8)分比(8.6±1.4)分(t=6.21,P<0.01),癌组织中的HMMR IRS高于癌旁组织为8.0(4.0,8.0)分比4.0(2.5,4.0)分(Z=3.94,P<0.01)。但不同ANLN、CYP2C9、HMMR蛋白表达水平对HCC患者术后复发时间及5年存活率影响差异无统计学意义(中位复发时间高水平比低水平:ANLN 38.6月比33.3月,CYP2C936.5月比35.5月,HMMR 33.1月比41.3月;中位生存时间高水平比低水平:ANLN 56.3月比51.1月,CYP2C955.1月比51.5月,HMMR 53.0月比55.2月;均P>0.05)。多因素Cox回归分析提示,BCLC、家族史对术后复发时间的影响差异有统计学意义(HR=2.435,P=0.025;HR=0.165,P=0.009),AFP、家族史与术后5年存活率独立相关(HR=229.488,P=0.041;HR=0.054,P=0.014)。结论ANLN、CYP2C9、HMMR蛋白表达水平在HCC患者癌组织及癌旁组织存在差异,但对预后未产生影响,提示其可作为HCC诊断的潜在标志物。展开更多
文摘Objective:Anillin(ANLN)is considered an oncogene in various cancers,but its effect on cervical cancer remains poorly understood.Hence,this study aimed to describe the action of ANLN on cervical cancer development and investigate the potential mechanism.Methods:Analysis of ANLN expression and its association with survival in carcinoma and endocervical adenocarcinoma(CESC)patients based on GEO and UALCAN databases.The tumor and adjacent normal tissues of 100 cervical cancer cases were harvested to detect the ANLN expression and explore its relationship with patient survival.Cell proliferation,apoptosis,migration,and invasion were measured by utilizing 5-ethynyl-2′-deoxyuridine(EdU)staining,Flow cytometry,and Transwell assay,respectively.ANLN andWnt expression were analyzed by RT-qPCR andWestern Blot.Results:ANLN was significantly elevated in tumor tissues,and cervical cancer cases with high ANLN expression exhibited poor survival and high dead proportion.Besides,ANLN induced cervical cancer cell proliferation,migration,and invasion and restrained cell apoptosis.In addition,ANLN promoted Wnt/β-catenin pathway activation.Furthermore,ANLN accelerated cell aggressive behaviors and suppressed cell apoptosis via activating the Wnt/β-catenin signaling in cervical cancer.Conclusion:ANLN was enhanced in cervical cancer tissues and related to poor prognosis.ANLN accelerated cervical cancer cell aggressive behaviors and suppressed cell apoptosis via activating theWnt/β-catenin pathway.
