STAT3 couples with 14-3-3σ to regulate BCR signaling,B-cell differentiation,and IgE production

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微小RNA-362在脑星形细胞瘤中的表达

目的研究微小RNA(microRNA,miR)-362在不同级别星形细胞瘤中的表达,探讨其临床意义及价值。方法使用定量聚合酶链反应(PCR)方法比较长治医学院附属和平医院32例星形细胞瘤患者和4例正常脑组织中miR-362的表达。多组间比较采用单因素方差分析,两组间比较使用配对t检验。结果所有星形细胞瘤组织miR-362表达(0.194±0.052)明显低于正常脑组织miR-362表达(0.436±0.044,t=8.887,P<0.05),差异有统计学意义,其中低级别星形细胞瘤组织miR-362表达(0.172±0.045)和高级别星形细胞瘤(0.202±0.070)均明显低于正常脑组织miR-362表达(t=10.101,t=6.386,P<0.05),差异有统计学意义,但低级别星形细胞瘤组织miR-362表达与高级别星形细胞瘤miR-362表达之间差异无统计学意义(t=1.284,P>0.05)。结论miR-362在星形细胞瘤组织中表达下调,但在低级别与高级别星形细胞瘤间无差异。     

Imatinib induces demethylation of miR-203 gene: An epigenetic mechanism of anti-tumor effect of imatinib

MicroRNA (miRNA) is an important regulator of cellular proliferation, differentiation and death. Leukemia-specific signature of miRNAs suggests that epigenetic dysregulation of miRNAs is important for leukemogenesis. We focused on the role of DNA methylation of miR-203 which targets BCR-ABL1 mRNA. The microarray analysis showed that 48 miRNAs of CpG-rich 212 miRNAs were upregulated over 2-fold after imatinib treatment. Imatinib induced the demethylation of the miR-203 promoter region, resulting in low expression of targeted BCR-ABL1 gene, and loss of proliferation of leukemic cells. In conclusion, demethylation of miR-203 is one of the molecular mechanisms of imatinib-induced inhibition of BCR-ABL1-positive leukemic cells.     

MicroRNA-mediated NBS1 gene silence and its effects on telomerase activation in Hela cells

Objective： To research the silence of NBS1 after transfection microRNA expressing eukaryotic recombinants and the changes of telomerase activation in telomerase-positive cell line Hela. Methods： According to the sequence of NBS1 mRNA, the NBS1 pre-microRNA was designed and synthesized, then cloned into the GFP reporter pcDNA6.2-GW/EmGFP-miR vector and transfected into Hela cells. The integrity of the insert fragment was verified through colony PCR and sequencing analysis. The NBS1 gene expression of NBS1 microRNA recombinants was detected by Real-Time PCR and western blot. Telomerase activity in Hela cells was assayed by TRAP-PCR-EB. Results： Sequences of insert fragment in microRNA expressing recombinants were correct. The NBS1 gene expression was decreased, and the telomerase activation of Hela cell reduced. Conclusion： NBS1 microRNA inhibits NBS1 gene expression, and depresses telomerase activation of Hela cells. This confirms that there is relevance between NBS 1 gene and telomerase activity.     

Evaluation of Serum microRNA Let-7c and Let-7d as Predictive Biomarkers for Metastatic Pancreatic Cancer

Background:First-line treatments for metastatic pancreatic cancer are chemotherapy regimens consisting of 5-fluorouracil or gemcitabine; however, there are no biomarkers to help determine which patients might benefit from which treatment regimens. We aimed to show that microRNAs let-7c and 7d can be used as independent predictive biomarkers for metastatic pancreatic cancer.Methods:A total of 55 patients who had first-line chemotherapy with FOLFIRINOX or gemcitabine + capecitabine were included. Patients were divided into groups based on let-7c and let-7d levels and chemotherapy treatment as let-7c-7d high FOLFIRINOX, let-7c-7d high gemcitabine + capecitabine, let-7c-7d low FOLFIRINOX, and let-7c-7d low gemcitabine + capecitabine. Blood samples were taken from patients before chemotherapy for microRNA let-7c and 7d analysis. MicroRNA isolation was performed using a miRNeasy Serum/Plasma Kit and identified using spectrophotometric measurements. After isolation, microRNA was converted to cDNA using a microRNA cDNA Synthesis Kit with poly (A) polymerase tailing. The expression of microRNA was examined using quantitative real-time polymerase chain reaction.Results:The overall survival of patients who received FOLFIRINOX treatment with a high let-7c-7d level was statistically significantly longer than those who received gemcitabine + capecitabine with a high let-7c-7d level. In addition, patients with low let-7c expression receiving FOLFIRINOX progressed significantly 2.104 times earlier than patients with high let-7c expression receiving FOLFIRINOX.Conclusion:The serum MicroRNA let-7c level was found to be an independent predictive biomarker in the FOLFIRINOX treatment group.     

结肠癌化疗耐药相关miRNA表达谱的初步研究

目的:应用基因芯片技术筛选结肠癌耐药相关微小RNAs (miRNAs),探究miRNAs对化疗耐药的调控机制。方法:采用基因芯片技术分析结肠癌细胞系HCT8及其耐长春新碱细胞系HCT8/v中miRNAs的表达差异,对部分差异表达的miRNAs应用RT-qPCR进行验证,对表达差异显著的miRNAs进行靶基因预测,利用Gene Ontology (GO)和京都基因与基因组百科全书(KEGG)数据库对预测到的靶基因进行生物信息学分析。结果:筛选出342个差异表达miRNAs,其中190个表达上调,152个表达下调。RT-qPCR验证结果示miR-125-5p、miR-181c-5p和miR-153-3的表达情况和芯片检测结果一致;miR-130a-3p和miR-149-3p的表达与芯片检测结果不一致。GO分析结果显示,耐药相关基因主要富集的旁路是RNA聚合酶II调控区序列特异性DNA结合旁路,主要通过正向调节发挥作用,位置主要是在细胞内有界细胞器上。KEGG分析结果显示,耐药相关基因最为富集的是轴突导向通路、胰岛素信号通路及磷脂酶D信号通路。结论:miRNAs与结肠癌化疗耐药密切相关。对这...     

外泌体miRNA在心血管疾病中的研究进展

<正>心血管疾病(cardiovascular diseases,CVD)是全球高发性疾病,其中冠心病(coronary heart disease,CHD)是世界范围内的主要死亡原因,在老年人群中死亡率和发病率不断上升[1],与微小RNA(microRNA,miRNA,miR)的调节密切相关[2]。研究报道,miRNA调节大量信号通路,可通过外泌体(exosome)实现细胞间传递,参与细胞间的信息交流[3],其严格     

microRNA let-7a在刀豆蛋白A诱导的小鼠肝损伤中的作用

目的:探讨microRNA let-7a对刀豆蛋白A(Concanavalin A,ConA)小鼠肝损伤的保护作用.方法:建立ConA诱导的小鼠肝损伤模型,采用尾静脉注射let-7a慢病毒表达质粒的方法,并在造模前7d给予let-7a进行治疗干预.采用自动生化仪分析检测血清ALT变化;ELISA检测血清TNF-α、IL-6和干扰素-γ(IFN-γ)表达水平;HE染色肝脏组织病理学观察,评价let-7a治疗效果.结果:治疗组血清ALT水平较模型组明显降低(P＜0.01);与模型组相比,治疗组IL-6水平明显降低(P＜0.01),治疗组血清炎症细胞因子TNF-α、IFN-γ水平也显著下降(P＜0.05).肝脏组织病理学检查显示,治疗组较模型组肝组织损伤程度明显减轻,炎症细胞明显减少(P＜0.01,P＜0.05).治疗组小鼠生存率明显高于模型组(P＜0.01).结论:let-7a对ConA诱导的小鼠肝损伤有保护作用,该作用可能通过抑制相关炎症细胞因子TNF-α、IL-6和IFN-γ表达来实现.     

外泌体miRNA在口腔疾病中的研究进展

外泌体是活细胞分泌至细胞外基质的纳米级囊泡,在细胞之间的物质交换和信号转导方面发挥重要作用,能将其携带的脂质、蛋白质、核酸传递至受体细胞,调节受体细胞的生理、病理过程。微小RNA(microRNA、miRNA)作为外泌体中重要的"货物"被转运至受体细胞,调控受体细胞信号通路,从而对疾病的进展起着调节的作用。近年来,外泌体miRNA在牙周疾病、黏膜相关疾病、口腔癌等疾病中的研究日益增多。本文就外泌体miRNA在口腔疾病中的调控机制进行综述,并讨论外泌体miRNA作为生物标志物在口腔疾病诊断中的潜在前景。     

Light Emitting Diodes Irradiation Regulates miRNA-877-3p to Promote Cardiomyocyte Proliferation

Mammalian cardiomyocytes (CMs) maintain a low capacity for self-renewal in adulthood, therefore the induction of CMs cycle re-entry is an important approach to promote myocardial repair after injury. Recently, photobiomodulation (PBM) has been used to manipulate physiological activities of various tissues and organs by non-invasive means. Here, we demonstrate that conditioned PBM using light-emitting diodes with a wavelength of 630 nm (LED-Red) was capable of promoting the proliferation of neonatal CMs. Further studies showed that low-power LED-Red affected the expression of miR-877-3p and promoted the proliferation of CMs. In contrast, silencing of miR-877-3p partially abolished the pro-proliferative actions of LED-Red irradiation on CMs. Mechanistically, GADD45g was identified as a downstream target gene of miR-877-3p. Conditioned LED-Red irradiation also inhibited the expression of GADD45g in neonatal CMs. Moreover, GADD45g siRNA reversed the positive effect of LED-Red on the proliferation of neonatal CMs. Taken together, conditioned LED-Red irradiation increased miR-877-3p expression and promoted the proliferation of neonatal CMs by targeting GADD45g. This finding provides a new insight into the role of LED-Red irradiation in neonatal CMs biology and suggests its potential application in myocardial injury repair.