检索结果-南通市图书馆

mir-29b suppresses the proliferation and migration of osteosarcoma cells by targeting CDK6

Protein & Cell 2016年第6期7卷 434-444页

作者： Kegan Zhu Lei Liu Junliang Zhang Yanbo Wang Hongwei Liang Gentao Fan Zhenhuan Jiang Chen-Yu Zhang Xi Chen Guangxin Zhou Department of Orthopedics School of Medicine Jinling Hospital Nanjing University Nanjing 210002 China State Key Laboratory of Pharmaceutical biotechnology.Collaborative Innovation Center ol Chemistry for Life Sciences NJU Advanced Institute for Life Sciences (NAILS) Jiangsu Engineering Research Center for MicroRNA Biology ando Biotechnology School of Life Sciences Nanjing University Nanjing 210046 China Department of Orthopedics The Affiliated Yixing Hospital of Jiangsu University Yixing 214200 China

Osteosarcoma is the most common primary sarcoma of bone, and it is a leading cause of cancer death among adolescents and young adults. However, the molecular mechanism underlying osteosarcoma carcinogenesis remains poorly understood. Recently, cyclin-dependent kinase 6 （CDK6） was identified as an important onco- gene. We found that CDK6 protein level, rather than CDK6 mRNA level, is much higher in osteosarcoma tissues than in normal adjacent tissues, which indicates a post-transcriptional mechanism involved in CDK6 regulation in osteosarcoma. mirNAs are small non- coding RNAs that repress gene expression at the post- transcriptional level and have widely been shown to play important roles in many human cancers. In this study, we investigated the role of mir-29b as a novel regulator of CDK6 using bioinformatics methods. We demon- strated that CDK6 can be downregulated by mir-29b via binding to the 3＇-UTR region in osteosarcoma cells. Furthermore, we identified an inverse correlation between mir-29b and CDK6 protein levels in osteosar- coma tissues. Finally, we examined the function of mir- 29b-driven repression of CDK6 expression in osteosarcoma cells. The results revealed that mir-29b acts as a tumor suppressor of osteosarcoma by targeting CDK6 in the proliferation and migration processes. Taken together, our results highlight an important role for mir-29b in the regulation of CDK6 in osteosarcoma and may open new avenues for future osteosarcoma therapies.

关键词： mir-29b osteosarcoma proliferation,migration tumorigenesis

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

mir-29b expression is altered in crescent formation of HSPN and accelerates AngⅡ-induced mesangial cell activation

引用

World Journal of Pediatrics 2020年第2期16卷 201-212页

作者： Shan Cheng Chun-Hua Zhu Ai-Hua Zhang Song-Ming Huang Department of Infectious Disease Children's Hospital of Nanjing Medical University72 Guangzhou RoadNanjing 210008China Department of Nephrology Children's Hospital of Nanjing Medical University72 Guangzhou RoadNanjing 210008China

background MicroRNA-29b(mir-29b)has been suggested to possess pro-inflammatory activity,which can partially be explained by the repression of tumor necrosis factor alpha protein three antibody(TNFAIP3).Meanwhile,it also promotes thyroid cell proliferation via Smad signaling *** present study aimed to elucidate the role of mir-29b in Henoch Sch(o)nlein purpura nephritis(HSPN)and its underlying molecular mechanism in angiotensinⅡ(AngⅡ)-induced human glomerular mesangial cell(HGMC)*** We evaluated mir-29b expression in 35 HSPN renal tissues based on crescent formation,glomerular sclerosis,interstitial fibrosis,thrombosis formation and capillary loop ***,HGMCs were cultured,treated with AngⅡand then transfected with LV-hsa-mir-29b-1 to induce mir-29b overexpression or LV-hsa-mir-29b-3p-inhibition to inhibit mir-29b ***,we examined the effects of mir-29b on cell proliferation and release of inflammatory *** We observed that mir-29b expression was significantly higher in the crescent group than in the no crescent ***-29b overexpression induced the release of intercellular adhesion molecule-1,interleukin-1β(IL-1β),IL-6,IL-8,the increase of CyclinA2,CyclinD 1,and cell *** also could inhibit the expressions of TNFAIP3 and NF-kappa-b-repressing factor(NKRF).Correspondingly,mir-29b inhibition produced the opposite effects and increased the expression of TNFAIP3 and *** mir-29b expression is altered in crescent formation of HSPN and accelerates AngⅡ-induced mesangial cell proliferation and release of inflammatory mediators.

关键词： Cell proliferation Crescent Inflammation mir-29b

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Exosomal mir-29b found in aqueous humour mediates calcium signaling in diabetic patients with cataract

引用

International Journal of Ophthalmology(English edition) 2021年第10期14卷 1484-1491页

作者： Chao Gao Xin Liu Fan Fan Jia-Ning Yang Xi-Yue Zhou Heng-Jun Mei Xiao-Lei Lin Yi Luo First Affiliated Hospital School of MedicineShihezi UniversityShihezi 832000Xinjiang Uygur Autonomous RegionChina Eye Institute Eye and ENT HospitalCollege of MedicineFudan UniversityShanghai 200031China State Key Laboratory of Medical Neurobiology Institutes of Brain Science and Collaborative Innovation Center for Brain ScienceShanghai Medical CollegeFudan UniversityShanghai 200031China Shanghai Key Laboratory of Visual Impairment and Restoration Science and Technology Commission of Shanghai MunicipalityShanghai 200031China Key Laboratory of Myopia(Fudan University) Chinese Academy of Medical SciencesNational Health CommissionShanghai 200031China

AIM:To investigate the role of exosomal mir-29b and Ca^(2+)in regulating the function of human lens epithelial cells(HLECs).METHODS:Exosomes were isolated from human aqueous humour(AH)by ultracentrifugation,and visualized by nanopar ticle tracking and transmission electron *** mirNA sequencing was performed to identify differentially expressed mirNAs between diabetes with cataracts(DMC)group and age-related cataracts(ARC)*** was used to predict potential target of certain *** expression of CACNA1C mRNA was determined by quantitative real-time polymerase chain reaction and CACNA1C protein was determined by Western *** of Ca^(2+)in human AH and the culture supernatant of cells were detected by the calcium assay *** counting kit-8 was used to determine cell ***:Exosomes were isolated from human AH,which had a typical cup-shaped phenotype and a particle size distribution in accordance with micro extracellular *** mirNA sequencing revealed that mir-29b was significantly downregulated in DMC group compared with ***^(2+)concentration of human AH in DMC was higher than that in *** culture supernatant of cells transfected with mir-29b inhibitors had a higher concentration of Ca^(2+)than that transfected with mir-29b ***-29b reduced the viability of HLECs by upregulating CACNA1C ***:Exosomes isolated from human AH contains abundant mirNAs.A significantly expressed mir NA,mir-29b,can affect the concentration of Ca^(2+)and regulate HLEC processes by upregulating CACNA1C.

关键词： exosomes mir-29b diabetes and cataracts Ca^(2+) CACNA1C

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Exercise attenuates angiotensinⅡ-induced muscle atrophy by targeting PPARγ/mir-29b

引用

Journal of Sport and Health Science 2022年第6期11卷 696-707,F0003页

作者： Qi Liu Liyang Chen Xuchun Liang Yuqing Cao Xinyue Zhu Siqi Wang Jin Li Juan Gao Junjie Xiao Cardiac Regeneration and Ageing Lab Institute of Cardiovascular SciencesSchool of Life ScienceShanghai UniversityShanghai 200444China Shanghai Engineering Research Center of Organ Repair School of MedicineShanghai UniversityShanghai 200444China

background:Exercise is beneficial for muscle *** proliferator-activated receptor gamma(PPARγ) and microRNA-29 b(mir-29 b) have been reported to be responsible for angiotensinⅡ(AngⅡ)-induced muscle ***,it is unclear whether exercise can protect AngⅡ-induced muscle atrophy by targeting PPARγ/mir-29 ***:Skeletal muscle atrophy in both the control group and the run group was established by AngⅡ infusion;after 1 week of exercise training,the mice were sacrificed,and muscle weight was *** size was measured by hematoxylin-eosin and wheat-germ agglutinin *** was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling *** expression level of muscle atrogenes,including F-box only protein 32(FbXO32,also called Atrogin-1) and muscle-specific RING-finger 1(MuRF-1),the phosphorylation level of protein kinase b(PKb,also called AKT)/forkhead box 03 A(FOX03 A)/mammalian target of rapamycin(mTOR) pathway proteins,the expression level of PPARγ and apoptosis-related proteins,including b-cell lymphoma-2(bcl-2),bcl-2-associated X(bax),cysteine-aspartic acid protease 3(caspase-3),and cleaved-caspase-3,were determined by western *** expression level of mir-29 b was checked by reversetranscription quantitative polymerase chain reaction.A PPARγ inhibitor(T0070907) or adeno-associated virus serotype-8(AAV8)-mediated mir-29 b overexpression was used to demonstrate whether PPARγ activation or mir-29 b inhibition mediates the beneficial effects of exercise in AngⅡ-induced muscle ***:Exercise can significantly attenuate AngⅡ-induced muscle atrophy,which is demonstrated by increased skeletal muscle weight,cross-sectional area of myofiber,and activation of AKT/mTOR signaling and by decreased atrogenes expressions and *** AngⅡ-induced muscle atrophy mice models,PPARγ was elevated whereas mir-29 b was decreased by *** protective effects of exercise in AngⅡ-induced muscle atrop

关键词： AngiotensinⅡ Exercise Muscle atrophy PPARg mir-29b

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

mir-29b upregulates mir-195 by targeting DNMT3b in tongue squamous cell carcinoma

引用

Science bulletin 2016年第3期61卷 212-219页

作者： Ling-Fei Jia Yun-Fei Zheng Ming-Yue Lyu Yi-Ping Huang Ye-Hua Gan Department of Oral and Maxillofacial Surgery PekingUniversity School and Hospital of Stomatology Beijing 100081China Central Laboratory Peking University School and Hospital ofStomatology Beijing 100081 China Department of Implantology Peking University School andHospital of Stomatology Beijing 100081 China Department of Orthodontics Peking University School andHospital of Stomatology Beijing 100081 China

MicroRNAs play important roles in the devel- opment and progression of various cancers, including tongue squamous cell carcinoma （TSCC）. mir-29b and mir-195 have been reported to be tumor suppressors in TSCC. Here, we investigated the expression of mir-29b and mir- 195 and their relationship in TSCC. Our data showed that mir-29b and mir-195 were significantly downregulated in TSCC com- pared with their matched nonmalignant tissues in 60 paired samples. The level of mir-29b was positively correlated with that of mir-195 in TSCC and the matched nonmalignant tissues. Moreover, mir-29b overexpression induced the demethylation of CpG islands upstream of mir-195 via targeting DNMT3b, leading to the upregulation of mir-195 in TSCC cell lines. Following DNMT3b silencing, the expression of mir-195 was increased and the methylation of CpG islands upstream of mir-195 was reduced. Although overexpression of mir-29b alone significantly increased mir- 195 expression, co-transfection of mir-29b with DNMT3b resulted in no change in mir-195 expression. Taken together, our results demonstrated that mir-29b could upregulate mir- 195 by directly targeting DNMT3b in TSCC. The interaction between mir-29b and mir-195 might provide new insights in developing novel therapeutic approaches of TSCC.

关键词： mirNA mir-29b mir-195 DNMT3b Tongue squamous cell carcinoma

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

mir-29b通过靶向PI3K/Akt信号通路降低胃癌细胞对顺铂的耐受性

引用

中国医学科学院学报 2015年第5期37卷 514-519页

作者：陈点点冯林春叶蕊何玉琦王雅棣中国人民解放军总医院放射治疗科北京100853 北京军区北戴河疗养院河北秦皇岛066100 北京军区总医院消化内科北京100700 北京军区总医院放射治疗科北京100700

目的探讨mir-29b与胃癌细胞顺铂耐受性之间的关系及其可能的调控机制。方法采用实时定量PCR(qRT-PCR)和Western blot法检测顺铂浓度梯度处理后胃癌细胞系中mir-29b及其靶基因的表达;CCK8法检测mir-29b敲低状态和过表达状态下胃癌细胞受... 详细信息

目的探讨mir-29b与胃癌细胞顺铂耐受性之间的关系及其可能的调控机制。方法采用实时定量PCR(qRT-PCR)和Western blot法检测顺铂浓度梯度处理后胃癌细胞系中mir-29b及其靶基因的表达;CCK8法检测mir-29b敲低状态和过表达状态下胃癌细胞受顺铂处理后的增殖情况,评估mir-29b对胃癌细胞顺铂耐受性的影响。结果顺铂处理后mir-29b表达量显著上调,其靶基因AKT2表达下调。过表达mir-29b后胃癌细胞对顺铂抗性下降,干扰mir-29b表达后对顺铂的耐受性增强。Rescue实验结果显示,mir-29b通过AKT2促使胃癌细胞发挥对顺铂抗性的拮抗作用。mir-29家族另外两个成员mir-29a/c受顺铂诱导上调表达,但二者对胃癌细胞顺铂抗性的产生无显著作用。结论 mir-29b能够通过靶向抑制PI3K/Akt信号通路降低胃癌细胞对顺铂的耐受性。

关键词：胃癌 mir-29b 顺铂抗性

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

mir-29b通过抑制N2a细胞p53凋亡通路减轻氧糖剥夺/再灌注损伤

引用

介入放射学杂志 2018年第5期27卷 451-457页

作者：陈立邹伟婕张宇张帅王黎洲周石贵州医科大学附属医院介入科贵阳550004

目的探讨微小核糖核酸(mir)-29b过表达是否抑制脑缺血损伤,进一步探讨其潜在机制。方法体外培养小鼠成神经细胞瘤N2a细胞,构建氧糖剥夺/再灌注(OGD/R)模型,模拟体外脑缺血损伤。N2a细胞随机分为空白对照组、OGD/R组、OGD/R+转染mir-29b... 详细信息

目的探讨微小核糖核酸(mir)-29b过表达是否抑制脑缺血损伤,进一步探讨其潜在机制。方法体外培养小鼠成神经细胞瘤N2a细胞,构建氧糖剥夺/再灌注(OGD/R)模型,模拟体外脑缺血损伤。N2a细胞随机分为空白对照组、OGD/R组、OGD/R+转染mir-29b激动剂组、OGD/R+转染mir-29b抑制剂组、转染mir-29b激动剂阴性对照组、转染mir-29b抑制剂阴性对照组。实时定量聚合酶链反应(RT-q PCR)检测各组mir-29b表达,溴化噻唑蓝四氮唑(MTT)比色法、乳酸脱氢酶(LDH)法检测mir-29b激动剂和抑制剂对OGD/R诱导细胞活性和凋亡的影响,Hoechst 33258染色法观察N2a细胞形态学特征及半胱氨酸天冬氨酸特异性蛋白酶(caspase)-3活性,免疫印迹法定量分析促凋亡蛋白bax、bcl-2及p53表达。结果经OGD/R处理的N2a细胞中mir-29b水平明显降低。mir-29b激动剂显著增加细胞活力,减少LDH漏出率,改善细胞核在凋亡过程中形态学变化,增强OGD/R条件下caspase-3活性;mir-29b抑制剂加剧OGD/R诱导的细胞毒性和细胞凋亡。mir-29b激动剂阻断OGD/R诱导的bax和p53蛋白表达增加,降低bcl-2蛋白表达;mir-29b抑制剂加剧OGD/诱导的这些凋亡相关蛋白改变。p53基因敲除的p53 si RNA降低细胞活力,增加LDH漏出率,逆转mir-29b激动剂对细胞损伤的改善作用。结论 mir-29b通过负调控p53依赖性凋亡途径减轻脑缺血性损伤,可能为缺血性脑卒中提供一潜在的治疗靶点。

关键词： mir-29b 脑缺血 p53基因细胞凋亡成神经细胞瘤N2a细胞

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

mir-29b通过靶向调节特异性蛋白1调控糖尿病性白内障晶状体上皮细胞间质转化的作用

引用

眼科新进展 2021年第12期41卷 1116-1121页

作者：牟琳刘苹李来岳娅婷西南医科大学附属中医医院眼科四川省泸州市646000

目的探究mir-29b通过靶向调节特异性蛋白1(SP-1)调控糖尿病性白内障晶状体上皮细胞间质转化(EMT)的作用机制。方法体外培养人晶状体上皮细胞(HLE-b3),分为正常组、高糖组、阴性组、mir-29b mimics组和mir-29b mimics+SP-1组。除正常组... 详细信息

目的探究mir-29b通过靶向调节特异性蛋白1(SP-1)调控糖尿病性白内障晶状体上皮细胞间质转化(EMT)的作用机制。方法体外培养人晶状体上皮细胞(HLE-b3),分为正常组、高糖组、阴性组、mir-29b mimics组和mir-29b mimics+SP-1组。除正常组细胞外,其余各组细胞于35.5 mmol·L^(-1)D-葡萄糖环境中培养。阴性组、mir-29b mimics组和mir-29b mimics+SP-1组分别共转染mirNA模拟物scramble和阴性siRNA序列、转染mir-29b模拟物、共转染mir-29b模拟物和SP-1基因序列。采用实时荧光定量PCR检测各组细胞mir-29b和SP-1 mRNA表达,采用Transwell法和细胞划痕实验检测各组细胞迁移活性。采用免疫荧光染色和Western blot检测和各组细胞钙黏蛋白(E-Cadherin、N-Cadherin)、波形蛋白(Vimentin)、SP-1蛋白表达情况。根据生物信息学数据库和双荧光素酶报告基因验证mir-29b和SP-1基因的靶向关系。结果35.5 mmol·L^(-1)D-葡萄糖组处理HLE-b324 h,细胞中mir-29b mRNA相对表达量较正常组降低,SP-1 mRNA和蛋白相对表达量均升高(均为Pmir-29b mimics组细胞mir-29b mRNA相对表达量和E-Cadherin蛋白表达增加,SP-1、N-Cadherin和Vimentin蛋白表达降低,细胞Transwell小室迁移数量和划痕愈合率均减少(均为Pmir-29b mimics+SP-1组较mir-29b mimics组细胞中E-Cadherin蛋白表达降低,N-Cadherin和Vimentin蛋白表达增加,细胞Transwell小室迁移数量和划痕愈合率增加(均为Pmir-29b mimics质粒可降低SP1-3’UTR-WT荧光素酶活性(P0.05)。结论mir-29b在糖尿病性白内障体外细胞模型中表达下调。上调mir-29b表达可通过靶向SP-1基因参与抑制高糖诱导晶状体上皮细胞EMT的进程。

关键词： mir-29b 调节特异性蛋白1 糖尿病白内障上皮细胞间质转化

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

mir-29b对人子宫内膜癌RL95-2细胞凋亡的影响

引用

基因组学与应用生物学 2019年第4期38卷 1944-1948页

作者：刘平韩新彦刘翠乔雯岚张易欣邯郸市中心医院邯郸56000

为了探讨mir-29b对人子宫内膜癌(endometrial cancer, EC) RL95-2细胞凋亡的影响及机制,本研究将RL95-2细胞转染mir-29b mimics和mir-NC后,采用MTT法检测细胞活力;运用Annexin V-PI法检测细胞凋亡;采用Western blotting检测Caspase-3蛋白表达;使用流式细胞术检测ROS水平。研究结果显示:与mir-NC组比较,mir-29b mimics过表达mir-29b组在培养24 h和48 h后的RL95-2细胞活力显著降低(pmir-NC组比较,mir-29b mimics组的RL95-2细胞凋亡率显著增加(pmir-NC组比较,mir-29b mimics组的RL95-2细胞Cleaved caspase-3蛋白表达水平显著增加(pmir-29b mimics组的RL95-2细胞ROS水平明显低于mir-NC组(pmir-29b可能通过调控ROS水平促进人RL95-2细胞凋亡。

关键词：子宫内膜癌 mir-29b 细胞凋亡 ROS

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

参芪扶正注射液通过调控mir-29b/bcl-2通路逆转胰腺癌多药耐药研究

引用

中草药 2021年第14期52卷 4262-4267页

作者：文柳静张洁天津医科大学肿瘤医院国家肿瘤临床医学研究中心天津市肿瘤防治重点实验室天津市恶性肿瘤临床医学研究中心天津300060

目的研究参芪扶正注射液对微小RNA-29b(microRNA-29b,mir-29b)和b淋巴细胞瘤2(b-cell lymphoma 2,bcl-2)表达的影响,探究参芪扶正注射液逆转胰腺癌多药耐药的可能机制。方法将mir-29b模拟物(mir-29b mimics)和mir-29b抑制剂(mir-29binhibitors)转染至人胰腺癌5-氟尿嘧啶(5-fluorouracil,5-Fu)耐药细胞株Patu8988/5-Fu,采用qRT-PCR检测参芪扶正注射液(5、10、20μL/mL)对Patu8988/5-Fu细胞mir-29bm RNA表达的影响;采用MTT法检测mir-29bmimics和mir-29binhibitors对Patu8988细胞活力的影响;采用Westernblotting法检测mir-29bmimics和mir-29b inhibitors对Patu8988/5-Fu细胞bcl-2蛋白表达的影响。结果与对照组比较,参芪扶正注射液组Patu8988/5-Fu细胞中mir-29b m RNA表达水平显著升高(Pmir-29b mimics组Patu8988/5-Fu细胞mir-29b mRNA表达水平显著升高(Pmir-29b inhibitors组mir-29b m RNA表达水平显著降低(Pmir-29b mimics组Patu8988细胞活力显著降低(Pmir-29b inhibitors组Patu8988细胞活力显著升高(Pmir-29b mimics组Patu8988/5-Fu细胞bcl-2蛋白表达水平显著降低(Pmir-29b mimics+参芪扶正注射液组bcl-2蛋白表达水平进一步降低(Pmir-29b inhibitors组Patu8988/5-Fu细胞bcl-2蛋白表达水平显著升高(Pmir-29b mimics+参芪扶正注射液组bcl-2蛋白水平无明显变化。结论 mir-29b通过下调bcl-2蛋白表达抑制Patu8988细胞增殖,参芪扶正注射液可能通过调控mir-29b/bcl-2通路从而逆转肿瘤多药耐药。

关键词：参芪扶正注射液胰腺癌 Patu8988/5-Fu 耐药性 mir-29b bcl-2

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：