Background： MicroRNAs （miRNAs） function as essential posttranscriptional modulators ofgene expression, and are involved in a wide range of physiologic and pathologic states, including cancer. Numerous miRNAs are de...Background： MicroRNAs （miRNAs） function as essential posttranscriptional modulators ofgene expression, and are involved in a wide range of physiologic and pathologic states, including cancer. Numerous miRNAs are deregulated in hepatocellular carcinoma （HCC）. This study aimed to investigate the role of miR-27a in the development of HCC. Methods： The expression of MiR-27a was measured by quantitative real-time polymerase chain reaction （qRT-PCR）. 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide was used to examine changes in the viability of HepG2, Bel-7402, Bel-7404 hepatoma cell lines associated with up-regulation or down-regulation of miR-27a. A dual-luciferase activity assay was used to verily a target gene ofmiR-27a, lmmunohistochemistry, qRT-PCR, Western blotting analysis, and cell cycle and apoptosis flow cytometric assays were used to elucidate the mechanism by which miR-27a modulates liver cancer cell proliferation. Results： The expression of miR-27a was significantly increased in HCC tissues and HepG2, Bel-7402, Bel-7404 hepatoma cell lines （P 〈 0.05）. We also found that the down-regulation of miR-27a in HepG2 cells dramatically inhibited proliferation, blocked the G1 to S cell cycle transition and induced apoptosis （P 〈 0.05）. In addition, miR-27a directly targeted the 3＇-untranslated region of peroxisonae proliferator-activated receptor y （PPAR-γ）, and ectopic miR-27a expression suppressed PPAR-γ expression on the mRNA and protein levels. The rosiglitazone-induced overexpression of PPAR-γ attenuated the effect of miR-27a in HCC cells. Conclusions： Our findings suggested that miRNA-27a promoted HCC cell proliferation by regulating PPAR-γ expression. MiR-27a may provide a potential therapeutic strategy for HCC treatment.展开更多
目的探讨通过超声造影和弹性成像联合血清miR-141、miR-27a水平构建的Logistic回归模型在乳腺肿块良恶性鉴别诊断中的价值。方法选择2020年8月至2022年9月于山西省人民医院就诊的98例乳腺肿块患者作为研究对象。对所有患者进行超声造影...目的探讨通过超声造影和弹性成像联合血清miR-141、miR-27a水平构建的Logistic回归模型在乳腺肿块良恶性鉴别诊断中的价值。方法选择2020年8月至2022年9月于山西省人民医院就诊的98例乳腺肿块患者作为研究对象。对所有患者进行超声造影和弹性成像检查,记录肿块弹性值(ultrasonic elastic value of mass,EvM)、周围脂肪弹性值(ultrasonic elastic value of tissue,EvT)、超声造影峰值强度(peak intensity,PI)、达峰时间(time to peak,TP)、平均度越时间(mean transit time,MTT)、肿块增强强度、增强均匀度、增强后病灶大小、显影时间、增强后有无放射性增强、有无穿支血流。应用定量实时聚合酶联反应法测定血清miR-141、miR-27a的表达水平。结果98例患者病灶中,63例为良性肿块,35例为恶性肿块。恶性组的超声造影高增强、显影时间早于周围组织、出现穿支血管和周围放射状增强的比例显著高于良性组(χ^(2)=19.36,6.71、19.06、10.28,P<0.001、0.010、<0.001、0.001)。恶性组的PI为17.20±3.04,显著高于良性组的15.02±1.95(t=3.83,P<0.001);恶性组TP为27.33±4.37,显著低于良性组的29.97±4.09(t=2.98,P=0.004)。恶性组的弹性成像参数EvM和EvT分别为(78.29±12.11)kPa和(13.13±2.56)kPa,均显著高于良性组的(50.07±9.61)kPa和(10.61±2.07)kPa,差异有统计学意义(t=11.33、2.62,P=<0.001、0.011)。恶性组的血清miR-141和miR-27a水平分别为(0.83±0.18)和(0.69±0.13),显著高于良性组的(0.61±0.13)和(0.50±0.07),差异有统计学意义(t=6.28、8.23,P均<0.001)。多因素Logistics回归分析结果显示增强强度、穿支血管、放射状增强、PI、EvM和血清miR-27a水平是乳腺恶性肿块的独立危险因素。Logistics回归模型诊断乳腺肿块良恶性的ROC曲线AUC为0.953(0.911~0.996),灵敏度和特异度分别为91.4%和88.9%。结论超声造影和弹性成像联合血清miR-141、miR-27a水平构建的Logistic回归模型在乳腺肿块良恶性�展开更多
Hypoxic injuries during fetal distress have been shown to cause reduced expression of micro RNA-27a（mi R-27a）,which regulates sensitivity of cortical neurons to apoptosis.We hypothesized that miR-27 a overexpression...Hypoxic injuries during fetal distress have been shown to cause reduced expression of micro RNA-27a（mi R-27a）,which regulates sensitivity of cortical neurons to apoptosis.We hypothesized that miR-27 a overexpression attenuates hypoxia- and ischemia-induced neuronal apoptosis by regulating FOXO1,an important transcription factor for regulating the oxidative stress response.miR-27 a mimic was transfected into hippocampal neurons to overexpress miR-27 a.Results showed increased hippocampal neuronal viability and decreased caspase-3 expression.The luciferase reporter gene system demonstrated that mi R-27 a directly binded to FOXO1 3′UTR in hippocampal neurons and inhibited FOXO1 expression,suggesting that FOXO1 was the target gene for mi R-27 a.These findings confirm that mi R-27 a protects hippocampal neurons against oxygen-glucose deprivation-induced injuries.The mechanism might be mediated by modulation of FOXO1 and apoptosis-related gene caspase-3 expression.展开更多
基金This study was supported by grants from Frontier Interdiscipline Program of Norman Bethune Health Science Center of Jilin University （No. 2013101001）, The Science and Technology Support Program of Jilin Province （No. 3D512K903430）, Young Scholars Program of Norman Bethune Health Science Center of Jilin University （No. 2013201011）, and the Nature Science Foundation of Jilin Province （No. 201215079）.
文摘Background： MicroRNAs （miRNAs） function as essential posttranscriptional modulators ofgene expression, and are involved in a wide range of physiologic and pathologic states, including cancer. Numerous miRNAs are deregulated in hepatocellular carcinoma （HCC）. This study aimed to investigate the role of miR-27a in the development of HCC. Methods： The expression of MiR-27a was measured by quantitative real-time polymerase chain reaction （qRT-PCR）. 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide was used to examine changes in the viability of HepG2, Bel-7402, Bel-7404 hepatoma cell lines associated with up-regulation or down-regulation of miR-27a. A dual-luciferase activity assay was used to verily a target gene ofmiR-27a, lmmunohistochemistry, qRT-PCR, Western blotting analysis, and cell cycle and apoptosis flow cytometric assays were used to elucidate the mechanism by which miR-27a modulates liver cancer cell proliferation. Results： The expression of miR-27a was significantly increased in HCC tissues and HepG2, Bel-7402, Bel-7404 hepatoma cell lines （P 〈 0.05）. We also found that the down-regulation of miR-27a in HepG2 cells dramatically inhibited proliferation, blocked the G1 to S cell cycle transition and induced apoptosis （P 〈 0.05）. In addition, miR-27a directly targeted the 3＇-untranslated region of peroxisonae proliferator-activated receptor y （PPAR-γ）, and ectopic miR-27a expression suppressed PPAR-γ expression on the mRNA and protein levels. The rosiglitazone-induced overexpression of PPAR-γ attenuated the effect of miR-27a in HCC cells. Conclusions： Our findings suggested that miRNA-27a promoted HCC cell proliferation by regulating PPAR-γ expression. MiR-27a may provide a potential therapeutic strategy for HCC treatment.
文摘目的探讨通过超声造影和弹性成像联合血清miR-141、miR-27a水平构建的Logistic回归模型在乳腺肿块良恶性鉴别诊断中的价值。方法选择2020年8月至2022年9月于山西省人民医院就诊的98例乳腺肿块患者作为研究对象。对所有患者进行超声造影和弹性成像检查,记录肿块弹性值(ultrasonic elastic value of mass,EvM)、周围脂肪弹性值(ultrasonic elastic value of tissue,EvT)、超声造影峰值强度(peak intensity,PI)、达峰时间(time to peak,TP)、平均度越时间(mean transit time,MTT)、肿块增强强度、增强均匀度、增强后病灶大小、显影时间、增强后有无放射性增强、有无穿支血流。应用定量实时聚合酶联反应法测定血清miR-141、miR-27a的表达水平。结果98例患者病灶中,63例为良性肿块,35例为恶性肿块。恶性组的超声造影高增强、显影时间早于周围组织、出现穿支血管和周围放射状增强的比例显著高于良性组(χ^(2)=19.36,6.71、19.06、10.28,P<0.001、0.010、<0.001、0.001)。恶性组的PI为17.20±3.04,显著高于良性组的15.02±1.95(t=3.83,P<0.001);恶性组TP为27.33±4.37,显著低于良性组的29.97±4.09(t=2.98,P=0.004)。恶性组的弹性成像参数EvM和EvT分别为(78.29±12.11)kPa和(13.13±2.56)kPa,均显著高于良性组的(50.07±9.61)kPa和(10.61±2.07)kPa,差异有统计学意义(t=11.33、2.62,P=<0.001、0.011)。恶性组的血清miR-141和miR-27a水平分别为(0.83±0.18)和(0.69±0.13),显著高于良性组的(0.61±0.13)和(0.50±0.07),差异有统计学意义(t=6.28、8.23,P均<0.001)。多因素Logistics回归分析结果显示增强强度、穿支血管、放射状增强、PI、EvM和血清miR-27a水平是乳腺恶性肿块的独立危险因素。Logistics回归模型诊断乳腺肿块良恶性的ROC曲线AUC为0.953(0.911~0.996),灵敏度和特异度分别为91.4%和88.9%。结论超声造影和弹性成像联合血清miR-141、miR-27a水平构建的Logistic回归模型在乳腺肿块良恶性�
基金supported by the National Natural Science Foundation of China,No.81101159the Natural Science Foundation of Jiangsu Province of China,No.BK20151268
文摘Hypoxic injuries during fetal distress have been shown to cause reduced expression of micro RNA-27a（mi R-27a）,which regulates sensitivity of cortical neurons to apoptosis.We hypothesized that miR-27 a overexpression attenuates hypoxia- and ischemia-induced neuronal apoptosis by regulating FOXO1,an important transcription factor for regulating the oxidative stress response.miR-27 a mimic was transfected into hippocampal neurons to overexpress miR-27 a.Results showed increased hippocampal neuronal viability and decreased caspase-3 expression.The luciferase reporter gene system demonstrated that mi R-27 a directly binded to FOXO1 3′UTR in hippocampal neurons and inhibited FOXO1 expression,suggesting that FOXO1 was the target gene for mi R-27 a.These findings confirm that mi R-27 a protects hippocampal neurons against oxygen-glucose deprivation-induced injuries.The mechanism might be mediated by modulation of FOXO1 and apoptosis-related gene caspase-3 expression.
