目的探究血清miR-135、miR-601、糖类抗原72-4(CA72-4)及糖类抗原19-9(CA19-9)的表达水平与胃癌(GC)诊断的相关性。方法选取2015年1月至2020年10月本院106例GC患者作为观察组,健康人群45例作为对照组,检测并比较两组血清miR-135、miR-60...目的探究血清miR-135、miR-601、糖类抗原72-4(CA72-4)及糖类抗原19-9(CA19-9)的表达水平与胃癌(GC)诊断的相关性。方法选取2015年1月至2020年10月本院106例GC患者作为观察组,健康人群45例作为对照组,检测并比较两组血清miR-135、miR-601、CA72-4及CA19-9表达水平;Pearson相关系数分析各指标与GC发生相关性;受试者工作特征(ROC)曲线评价各指标对GC诊断效能。结果与对照组比较,观察组血清miR-135、miR-601、CA72-4及CA19-9表达水平升高差异有统计学意义(P<0.05);血清miR-135、miR-601、CA72-4及CA19-9与GC的发生呈正相关(P<0.05);血清miR-135、miR-601、CA72-4及CA19-9联合诊断GC灵敏度、特异性、准确度,阳性预测值、阴性预测值、ROC曲线下面积(area under curve,AUC)显著高于单一指标(P<0.05)。结果血清miR-135、miR-601、CA72-4及CA19-9的表达水平与GC的发生呈正相关。展开更多
背景与目的:胃癌是消化内科常见的恶性肿瘤。探讨血清miR-135及miR-601在胃癌患者中的表达及其诊断价值。方法:选取2016年1月1日-2019年9月30日三亚中心医院收治的胃癌患者152例,根据胃癌病情进展及临床病理学分期分为早期胃癌组(n=62)...背景与目的:胃癌是消化内科常见的恶性肿瘤。探讨血清miR-135及miR-601在胃癌患者中的表达及其诊断价值。方法:选取2016年1月1日-2019年9月30日三亚中心医院收治的胃癌患者152例,根据胃癌病情进展及临床病理学分期分为早期胃癌组(n=62)和进展期胃癌组(n=90),Ⅰ~Ⅱ期(n=65)和Ⅲ~Ⅳ期(n=87),无淋巴结转移组(n=73)和淋巴结转移组(n=79)。另选择96例非胃癌患者作为非胃癌组,60例健康体检正常者作为对照组。采用实时荧光定量聚合酶链反应(real-time fluorescence quantitative polymerase chain reaction,RTFQ-PCR)检测各组血清miR-135及miR-601表达水平,化学发光法测定糖类抗原72-4(carbohydrate antigen 72-4,CA72-4)及糖类抗原19-9(carbohydrate antigen 19-9,CA19-9)水平,分析其对早期胃癌的诊断价值。采用Pearson相关分析来分析胃癌患者血清miR-135、miR-601水平与CA72-4及CA19-9的相关性。结果:与非胃癌组和对照组比较,胃癌组血清miR-135、miR-601、CA72-4及CA19-9水平均明显升高(P均<0.001)。进展期胃癌组血清miR-135(5.70±1.84 vs 3.83±1.12)、miR-601(11.28±3.73 vs 7.36±2.15)、CA72-4[(41.75±10.14)U/mL vs(17.82±4.93)U/mL]及CA19-9[(63.72±17.50)U/mL vs(35.84±10.36)U/mL]水平均明显高于早期胃癌组(均P<0.001)。Ⅲ~Ⅳ期胃癌患者血清miR-135(6.10±1.90 vs 3.74±1.08)、miR-601(12.14±3.92 vs 7.05±2.04)、CA72-4[(44.68±12.35)U/mL vs(16.40±4.52)U/mL]和CA19-9[(68.53±19.13)U/mL vs(33.75±10.60)U/mL]水平均明显高于Ⅰ~Ⅱ期(均P<0.001),而且Ⅱ期胃癌患者血清miR-135、miR-601、CA72-4及CA19-9水平均明显高于对照组(P<0.05)。淋巴结转移组血清miR-135(6.24±1.95 vs 3.65±0.97)、miR-601(12.60±4.13 vs 6.84±1.92)、CA72-4[(48.70±12.37)U/mL vs(14.85±4.20)U/mL]和CA19-9[(72.36±20.25)U/mL vs(31.60±10.17)U/mL]水平均明显高于无淋巴结转移组(均P<0.001)。受试者工作特征(receiver operating characteristic,ROC)曲线分析结果显示,血清miR-135、miR-601、CA72-4及展开更多
目的:检测miR-224与miR-135a两种microRNA(miRNA)在非小细胞肺癌中的表达,探讨其与肺癌临床病理的关系。方法:采用Real time RT-PCR法对31例非小细胞肺癌组织及癌旁正常肺组织的miR-224与miR-135a进行定量分析,结果由2(-△△CT)处理,并...目的:检测miR-224与miR-135a两种microRNA(miRNA)在非小细胞肺癌中的表达,探讨其与肺癌临床病理的关系。方法:采用Real time RT-PCR法对31例非小细胞肺癌组织及癌旁正常肺组织的miR-224与miR-135a进行定量分析,结果由2(-△△CT)处理,并分析与临床病理资料的关系。结果:相对内参U6,miR-224在非小细胞肺癌组织中表达量为4.2761±0.8731,在正常肺组织中的表达量为0.8967±0.2154,两者相比P<0.05,miR-135a在非小细胞肺癌组织中表达量为0.3551±0.0985,在正常肺组织中的表达量为1.7443±0.3125,两者相比P<0.05。miR-224与miR-135a的表达与非小细胞肺癌的临床分期、病理分级密切相关。结论:miR-224高表达及miR-135a低表达与非小细胞肺癌的临床分期、病理分级密切相关,miR-224有可能作为非小细胞肺癌的重要肿瘤标志物。展开更多
Cellular microRNAs(miRNAs) have been shown to modulate HCV infection via directly acting on the viral genome or indirectly through targeting the virus-associated host factors. Recently we generated a comprehensive map...Cellular microRNAs(miRNAs) have been shown to modulate HCV infection via directly acting on the viral genome or indirectly through targeting the virus-associated host factors. Recently we generated a comprehensive map of HCV–miRNA interactions through genome-wide miRNA functional screens and transcriptomics analyses. Many previously unappreciated cellular miRNAs were identified to be involved in HCV infection, including miR-135a, a human cancerrelated miRNA. In the present study, we investigated the role of miR-135a in regulating HCV life cycle and showed that it preferentially enhances viral genome replication. Bioinformatics-based integrative analyses and subsequent functional assays revealed three antiviral host factors, including receptor interacting serine/threonine kinase 2(RIPK2), myeloid differentiation primary response 88(MYD88), and C-X-C motif chemokine ligand 12(CXCL12), as bona fide targets of miR-135a. These genes have been shown to inhibit HCV infection at the RNA replication stage. Our data demonstrated that repression of key host restriction factors mediated the proviral effect of miR-135a on HCV propagation. In addition,miR-135a hepatic abundance is upregulated by HCV infection in both cultured hepatocytes and human liver, likely mediating a more favorable environment for viral replication and possibly contributing to HCV-induced liver malignancy.These results provide novel insights into HCV–host interactions and unveil molecular pathways linking miRNA biology to HCV pathogenesis.展开更多
文摘目的探究血清miR-135、miR-601、糖类抗原72-4(CA72-4)及糖类抗原19-9(CA19-9)的表达水平与胃癌(GC)诊断的相关性。方法选取2015年1月至2020年10月本院106例GC患者作为观察组,健康人群45例作为对照组,检测并比较两组血清miR-135、miR-601、CA72-4及CA19-9表达水平;Pearson相关系数分析各指标与GC发生相关性;受试者工作特征(ROC)曲线评价各指标对GC诊断效能。结果与对照组比较,观察组血清miR-135、miR-601、CA72-4及CA19-9表达水平升高差异有统计学意义(P<0.05);血清miR-135、miR-601、CA72-4及CA19-9与GC的发生呈正相关(P<0.05);血清miR-135、miR-601、CA72-4及CA19-9联合诊断GC灵敏度、特异性、准确度,阳性预测值、阴性预测值、ROC曲线下面积(area under curve,AUC)显著高于单一指标(P<0.05)。结果血清miR-135、miR-601、CA72-4及CA19-9的表达水平与GC的发生呈正相关。
文摘背景与目的:胃癌是消化内科常见的恶性肿瘤。探讨血清miR-135及miR-601在胃癌患者中的表达及其诊断价值。方法:选取2016年1月1日-2019年9月30日三亚中心医院收治的胃癌患者152例,根据胃癌病情进展及临床病理学分期分为早期胃癌组(n=62)和进展期胃癌组(n=90),Ⅰ~Ⅱ期(n=65)和Ⅲ~Ⅳ期(n=87),无淋巴结转移组(n=73)和淋巴结转移组(n=79)。另选择96例非胃癌患者作为非胃癌组,60例健康体检正常者作为对照组。采用实时荧光定量聚合酶链反应(real-time fluorescence quantitative polymerase chain reaction,RTFQ-PCR)检测各组血清miR-135及miR-601表达水平,化学发光法测定糖类抗原72-4(carbohydrate antigen 72-4,CA72-4)及糖类抗原19-9(carbohydrate antigen 19-9,CA19-9)水平,分析其对早期胃癌的诊断价值。采用Pearson相关分析来分析胃癌患者血清miR-135、miR-601水平与CA72-4及CA19-9的相关性。结果:与非胃癌组和对照组比较,胃癌组血清miR-135、miR-601、CA72-4及CA19-9水平均明显升高(P均<0.001)。进展期胃癌组血清miR-135(5.70±1.84 vs 3.83±1.12)、miR-601(11.28±3.73 vs 7.36±2.15)、CA72-4[(41.75±10.14)U/mL vs(17.82±4.93)U/mL]及CA19-9[(63.72±17.50)U/mL vs(35.84±10.36)U/mL]水平均明显高于早期胃癌组(均P<0.001)。Ⅲ~Ⅳ期胃癌患者血清miR-135(6.10±1.90 vs 3.74±1.08)、miR-601(12.14±3.92 vs 7.05±2.04)、CA72-4[(44.68±12.35)U/mL vs(16.40±4.52)U/mL]和CA19-9[(68.53±19.13)U/mL vs(33.75±10.60)U/mL]水平均明显高于Ⅰ~Ⅱ期(均P<0.001),而且Ⅱ期胃癌患者血清miR-135、miR-601、CA72-4及CA19-9水平均明显高于对照组(P<0.05)。淋巴结转移组血清miR-135(6.24±1.95 vs 3.65±0.97)、miR-601(12.60±4.13 vs 6.84±1.92)、CA72-4[(48.70±12.37)U/mL vs(14.85±4.20)U/mL]和CA19-9[(72.36±20.25)U/mL vs(31.60±10.17)U/mL]水平均明显高于无淋巴结转移组(均P<0.001)。受试者工作特征(receiver operating characteristic,ROC)曲线分析结果显示,血清miR-135、miR-601、CA72-4及
文摘目的:检测miR-224与miR-135a两种microRNA(miRNA)在非小细胞肺癌中的表达,探讨其与肺癌临床病理的关系。方法:采用Real time RT-PCR法对31例非小细胞肺癌组织及癌旁正常肺组织的miR-224与miR-135a进行定量分析,结果由2(-△△CT)处理,并分析与临床病理资料的关系。结果:相对内参U6,miR-224在非小细胞肺癌组织中表达量为4.2761±0.8731,在正常肺组织中的表达量为0.8967±0.2154,两者相比P<0.05,miR-135a在非小细胞肺癌组织中表达量为0.3551±0.0985,在正常肺组织中的表达量为1.7443±0.3125,两者相比P<0.05。miR-224与miR-135a的表达与非小细胞肺癌的临床分期、病理分级密切相关。结论:miR-224高表达及miR-135a低表达与非小细胞肺癌的临床分期、病理分级密切相关,miR-224有可能作为非小细胞肺癌的重要肿瘤标志物。
基金supported by the Intramural Research Program of the National Institute of Diabetes and Digestive and Kidney Diseases, US National Institutes of Health
文摘Cellular microRNAs(miRNAs) have been shown to modulate HCV infection via directly acting on the viral genome or indirectly through targeting the virus-associated host factors. Recently we generated a comprehensive map of HCV–miRNA interactions through genome-wide miRNA functional screens and transcriptomics analyses. Many previously unappreciated cellular miRNAs were identified to be involved in HCV infection, including miR-135a, a human cancerrelated miRNA. In the present study, we investigated the role of miR-135a in regulating HCV life cycle and showed that it preferentially enhances viral genome replication. Bioinformatics-based integrative analyses and subsequent functional assays revealed three antiviral host factors, including receptor interacting serine/threonine kinase 2(RIPK2), myeloid differentiation primary response 88(MYD88), and C-X-C motif chemokine ligand 12(CXCL12), as bona fide targets of miR-135a. These genes have been shown to inhibit HCV infection at the RNA replication stage. Our data demonstrated that repression of key host restriction factors mediated the proviral effect of miR-135a on HCV propagation. In addition,miR-135a hepatic abundance is upregulated by HCV infection in both cultured hepatocytes and human liver, likely mediating a more favorable environment for viral replication and possibly contributing to HCV-induced liver malignancy.These results provide novel insights into HCV–host interactions and unveil molecular pathways linking miRNA biology to HCV pathogenesis.
