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mir-21, mir-221 and mir-222 expression and prostate cancer recurrence among obese and non-obese cases

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Asian Journal of Andrology 2013年第2期15卷 226-230,I0007页

作者： Ernest K Amankwah Evelyn Anegbe Hyun Park Julio Pow-Sang Ardeshir Hakam Jong Y Park Department of Cancer Epidemiology H. Lee Moffitt Cancer Center Tampa FL 33612 USA Department of G U Oncology H. Lee Moffitt Cancer Center Tampa FL 33612 USA Department of Anatomic Pathology H. Lee Moffitt Cancer Center Tampa FL 33612 USA

Recent evidence shows that certain microRNAs （mirNAs） play a role in both obesity and prostate cancer recurrence, but the association between the expression of these mirNAs and obesity in prostate cancer recurrence is unknown. In this study, we examined the effect of the interaction between obesity and mir-21, mir-221 or mir-222 expression on prostate cancer recurrence among 28 recurrent and 37 non-recurrent prostate cancer cases, mirNA expression was determined using quantitative real-time polymerase chain reaction. Cox proportional hazard models adjusting for age at diagnosis, clinical stage and Gleason score were used to estimate hazard ratios （HR） and 95% confidence intervals （95% CI） for recurrence free survival. A significantly （P=0.014） higher proportion of recurrent cases （78,6%） than non-recurrent cases （48.6%） had a low expression of mir-21 and the difference was more prominent in obese than non-obese patients. Multivariate analysis showed that the expression of mir-21 was an independent risk factor for recurrence in obese （HR=6.15, 95% CI= 1.04-36.48, P=-0.045）, but not in non-obese （HR= 1.28, 95% C1=0.30-5.49, P=0.74） cases. A significant association with recurrence was not observed for the expression of mir-221 and mir-222. In summary, our findings show that mir-21 is associated with prostate cancer recurrence after radical prostatectomy and suggest that the differential expression of mir-21 is more prominent in obese than in non-obese cases. Future larger studies are warranted to confirm these initial findings and to elucidate the mechanisms involved.

关键词： mir-21 mir-221 mir-222 mirNA obesity prostate carcinoma recurrence

mir-222 Inhibits Migration And chemotaxis of TAMs to Breast Tumor

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MiR-222 Inhibits Migration And chemotaxis of TAMs to Breast ...

mir-222对山羊副流感病毒3型复制的影响

第九届全国免疫学学术大会

作者： Zhao Lianmei Shijiuan Li Lingxue Liu Yanxin Shan Baoen Zheng Dexian State Key Laboratory of Medical Molecular Biology School of Basic MedicinePeking Union Medical CollegeInstitute of Basic Medical SciencesChinese Academy of Medical Sciences Research center The fourth hospital of Hebei medical university

Macrophages are found in majority of malignant *** object of this study is to evaluate the effect of mmumir-222 on infiltration of macrophages to breast tumor andstudy the mechanisms ofmmu-mir-222 in ***:We detected the expression level of mir-222,mir-221 and mir-31 in TAM and macrophage from normal PBMC(Peripheral blood mononuclear cells)using real *** further verified them in mouse TAM derived from tumor formed by4T1 cells and macrophages fromthe abdominal cavity of *** investigated the effect of mir-222 on mRNA expression level of cytokines and chemokines associated with M2 macrophage,including IL-17A,CCL17,CCL5,CCL21and TGF-beta by ***,lentivirus(LV)vector encoding mmu-mir-222was constructed and cell line of RAW264.7 was stably infected with the lentivirus followed by flow cytometry *** investigated the proliferation of RAW264.7-mir-222-overexpressing and control RAW264.7 using MTS assays and migration of two group’s cell using transwell chamber *** injected the RAW264.7-mir-222-and control RAW264.7 to mouse subcutaneously and investigated the tumor ***,we compared the ability of migration of two group’s cells to tumor in mouse and detect the number of RAW264.7 to tumor using flow ***:mir-222,mir-221 are downregulated in TAM compared with macrophage derived from PBMC or that fromthe abdominal cavity whearas mir-31is overexpressed in TAM,consisting with our previous mirNA chip *** mouse peritoneal macrophages were transfected with chemically synthesized mmu-mir-222 mimics for 24 h followed by stimulation with LPS for 12 h,the expression of CCL5 and CCL17 which are the feature molecules of M2,weredecreased,and wereup-regulated comparedwith the cells transfected with mmu-mir-222 ***,lentivirus(LV)vector encoding mmu-mir-222was constructed successfully and mir-222 was increased by 5.63 ***,RAW264.7-mir-222 had a reduced number of metabolicallyacti

关键词： mir-222 TAM chemotaxis breast tumor RAW264.7

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畜牧兽医学报 2018年第12期49卷 2664-2671页

作者：钟纯燕李基棕毛立李文良郝飞孙敏刘茂军主性嵇辛勤肖芳杨蕾蕾张纹纹江苏省农业科学院兽医研究所农业部兽用生物制品工程技术重点实验室南京210014 临沂大学药学院临沂276000 贵州大学动物科学学院贵阳550025

为探讨mir-222对山羊副流感病毒3型(CPIV3)复制的影响及其机制。本研究将mir-222模拟体转染MDBK细胞,接种CPIV3病毒液,收集上清和细胞,测定病毒效价和干扰素(IFN)含量;通过Target Scan和miranda等生物信息学软件预测mir-222调控的靶基因... 详细信息

为探讨mir-222对山羊副流感病毒3型(CPIV3)复制的影响及其机制。本研究将mir-222模拟体转染MDBK细胞,接种CPIV3病毒液,收集上清和细胞,测定病毒效价和干扰素(IFN)含量;通过Target Scan和miranda等生物信息学软件预测mir-222调控的靶基因,用双荧光素酶报告系统验证其靶基因,RNA干扰技术研究靶基因对CPIV3复制的影响。结果显示,mir-222模拟体能抑制CPIV3复制,转染mir-222组IFN的表达水平较高,且病毒复制效价(10^(2. 5)TCID_(50)·0. 1 mL^(-1))显著低于mirNA阴性对照组(10^(3. 3)TCID_(50)·0. 1 mL^(-1));双荧光素酶报告系统验证和qPCR检测得出,mir-222可靶向结合IRF2的3'-UTR,并降解IRF2的mRNA和抑制IRF2蛋白表达;敲除IRF2的MDBK细胞感染CPIV3后,病毒复制效价(10^(2. 0)TCID_(50)·0. 1 mL^(-1))低于正常MDBK细胞组(10^(3. 2)TCID_(50)·0. 1 mL^(-1))。本研究表明,mir-222通过靶向降解IRF2 mRNA提高IFN表达水平来抑制CPIV3复制,为基于mir-222研制潜在抗病毒药物提供基础资料。

关键词：山羊副流感病毒3型 mir-222 MDBK细胞 IRF2

mir-222通过靶向RB1促进视网膜母细胞瘤细胞生长与侵袭

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中国癌症杂志 2016年第9期26卷 743-749页

作者：刘越峰张勇钟晓东罗卫民湖北医药学院附属十堰市太和医院眼科中心湖北十堰442000 湖北医药学院附属十堰市太和医院心胸外科湖北十堰442000

背景与目的:视网膜母细胞瘤基因1(retinoblastoma 1,RB1)能够抑制多种肿瘤的发生、发展,且与细胞周期、分化、衰老、凋亡及生长抑制等调控密切相关。该研究旨在明确mir-222是否通过靶向RB1表达而促进视网膜母细胞瘤细胞的生长与侵袭,进... 详细信息

背景与目的:视网膜母细胞瘤基因1(retinoblastoma 1,RB1)能够抑制多种肿瘤的发生、发展,且与细胞周期、分化、衰老、凋亡及生长抑制等调控密切相关。该研究旨在明确mir-222是否通过靶向RB1表达而促进视网膜母细胞瘤细胞的生长与侵袭,进一步揭示mir-222促瘤作用的分子机制。方法:将mir-222(mir-222模拟物)+RB1-wt(野生型RB1的3’-非翻译区的荧光素酶报告载体)、mir-NC(无关序列对照)+RB1-wt、mir-222+RB1-mut(突变型RB1的3’-非翻译区的荧光素酶报告载体)及mir-NC+RB1-mut共转染人视网膜母细胞瘤细胞株Y79,并采用单光子检测荧光素酶活性。采用蛋白[质]印迹法(Western blot)检测RB1表达水平的改变。将mir-222与mir-NC、RB1(pc DNA3.1-RB1)与vector(pc DNA3.1)、mir-222+RB1及mir-NC+vector转染Y79细胞,MTS检测细胞生长增殖活性,Transwell侵袭实验检测Y79细胞生长与侵袭能力的影响。结果:与mir-NC+RB1-wt组比较,共转染mir-222+RB1-wt组的荧光素酶活性强度降低了约56.67%(Pmir-NC比较,mir-222组RB1蛋白水平显著下调(Pmir-222组细胞生长速度显著高于mir-NC组(Pmir-222+pc DNA3.1-RB1组和mir-NC+pc DNA3.1组比较,细胞生长速度差异无统计学意义(P>0.05)。转染mir-222组穿过基底膜的细胞数分别为(193±10),与对照组(144±11)比较能明显加快Y79细胞的穿膜能力,差异有统计学意义(Pmir-NC+pc DNA3.1组和mir-222+pc DNA3.1-RB1组比较,穿过基底膜的细胞数差异无统计学意义(P>0.05)。结论:mir-222通过靶向调控RB1表达而促进视网膜母细胞瘤细胞的生长与侵袭。

关键词：视网膜母细胞瘤 mir-222 RB1 生长侵袭

mir-222对奶牛乳腺上皮细胞乳脂代谢的影响研究

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吉林农业大学学报 2023年

作者：邓耿高苗丰帅高振于海滨姜平赵志辉广东海洋大学滨海农业学院

乳腺是犊牛生长所需营养物质和抗体的外分泌腺体，其内部汇集大量具有泌乳功能的腺泡。腺泡周围的乳腺上皮细胞(mammaryepithelialcells，MECs)以单层而紧密的方式排列，它是乳腺中合成和分泌乳汁的基本单元，也是乳腺对外界病原进行免... 详细信息

乳腺是犊牛生长所需营养物质和抗体的外分泌腺体，其内部汇集大量具有泌乳功能的腺泡。腺泡周围的乳腺上皮细胞(mammaryepithelialcells，MECs)以单层而紧密的方式排列，它是乳腺中合成和分泌乳汁的基本单元，也是乳腺对外界病原进行免疫保护的重要组分。乳汁正是在MECs内由血液中的各类营养物质经过一系列复杂生化过程而形成。mir-222作为在高脂和低脂中国荷斯坦奶牛中显著差异性表达的mirNAs，其在牛乳腺上皮细胞（bMECs）中的功能尚不清楚。因此，本研究旨在明确mir-222对奶牛乳腺上皮细胞乳脂代谢的影响，通过将mir-222的过表达和干扰载体分别转染进bMECs中，检测bMECs内甘油三酯、胆固醇，同时对bMECs的增殖和凋亡能力进行检测，结果显示：与mir-shNC组相比，过表达mir-222可显著降低细胞内甘油三酯含量（Pmir-222不仅参与调控bMECs的命运，还参与调控bMECs的乳脂合成以及脂肪酸代谢过程，为深入探讨mir-222 在bMECs乳脂代谢中的调控作用和分子机制奠定基础。

关键词： mir-222 牛乳腺上皮细胞细胞增殖与凋亡乳脂代谢

mir-222通过下调DDIT4抑制肾癌细胞自噬

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中国癌症杂志 2015年第3期25卷 161-166页

作者：倪晓辰赵志红马永良任宗涛刘彬张爱莉河北医科大学第四医院泌尿外科河北石家庄050011

背景与目的:微小RNA(microRNA,mirNA,mir)在肿瘤的发生、发展中具有重要的作用。mir-222在多种肿瘤组织中表达上调,而其在肾癌(renal cell carcinoma,RCC)中的表达及其作用机制尚不清楚。本研究拟通过检测RCC组织及相应癌旁组织中mir-22... 详细信息

背景与目的:微小RNA(microRNA,mirNA,mir)在肿瘤的发生、发展中具有重要的作用。mir-222在多种肿瘤组织中表达上调,而其在肾癌(renal cell carcinoma,RCC)中的表达及其作用机制尚不清楚。本研究拟通过检测RCC组织及相应癌旁组织中mir-222的表达情况,探讨mir-222在RCC中的作用。并在体外条件下,通过检测mir-222的下游作用靶点,探讨mir-222的抗RCC作用机制。方法:采用实时定量聚合酶链反应(quantitative real-time polymerase chain reaction,qRT-PCR)检测RCC组织和癌旁组织中mir-222的表达;采用CCK-8法检测细胞的增殖活力;采用蛋白[质]印迹法(Western blot)检测DDIT4蛋白及LC3-Ⅱ的表达;采用荧光素酶实验验证mir-222的作用靶点;转染EGFF-LC3后在激光共聚焦显微镜下观察细胞自噬状态。结果:qRTPCR检测结果显示,mir-222在RCC组织中表达明显上调。在人肾透明细胞癌786-O细胞株中敲低mir-222表达后显著抑制细胞的增殖活力,而过表达mir-222可增强786-O细胞的增殖活力(Pmir-222后,其靶基因DDIT4蛋白的表达显著上调,过表达mir-222后,DDIT4表达明显下调。荧光素酶实验结果表明,DDIT4为mir-222的直接作用靶点。RCC组织的DDIT4表达下调。在786-O细胞中抑制mir-222表达后,LC3-Ⅱ的表达水平显著上调,自噬体数目显著增加。结论:mir-222在RCC中高表达,并可能通过靶向抑制DDIT4的表达参与调控RCC细胞自噬。

关键词： mir-222 肾癌 DDIT4 自噬

mir-222 Inhibits Migration And Chemotaxis of TAM to Breast cancer

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miR-222 Inhibits Migration And Chemotaxis of TAM to Breast c...

mir-222在胃癌中的表达分析及其靶基因FOS的鉴定

第九届全国免疫学学术大会

Object:Macrophages are found in majority of malignant *** object of this study is to evaluate the effect of mir-222 on infiltration of macrophage to breast cancer and study the molecular mechanisms ofmir-222 in ***:We investigated the effect of mir-222 on mRNA expression level of cytokines associated with M2 macrophage,including IL-17A,CCL17,CCL5,CCL21 and TGF-beta by ***,lentivirus(LV)vector encoding mmu-mir-222 was constructed and cell line of RAW264.7 was stably infected with the lentivirus followed by flow cytometry *** investigated the proliferation of RAW264.7-mir-222-overexpressing and control RAW264.7using MTS assays and migration of two group’s cell using transwell chamber ***264.7-mir-222-and control RAW264.7 was injected to mouse subcutaneously and the tumor formation was ***,we compared the ability of migration of two groups’cells to tumor in mouse using flow ***:When mouse peritoneal macrophages were transfected with chemically synthesized mir-222 mimics for 24 h followed by stimulation with LPS for 12 h,the expression of CCL5 and CCL17 were decreased,and they are up-regulated compared with the cells transfected with mmu-mir-222 ***-222 was stably increased expression in RAW264.7 by5.63 fold ***,RAW264.7-mir-222 had a reduced number of metabolically active cells to tumor in mouse compared with control RAW264.7 *** was also showed that ectopic expression of mir-222 decreased the migration and invasion ability of RAW264.7 in ***:mir-222 inhibits the M2 macrophages proliferation and migrated to tumor partly through suppressing CCL5 and CCL17 chemokines release.

关键词： mir-222 TAM chemotaxis breast cancer RAW264.7

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第三军医大学学报 2010年第24期32卷 2577-2581页

作者：朱恩东李娜肖斌黎伯胜毛旭虎邹全明第三军医大学医学检验系临床微生物学及免疫学教研室国家免疫生物制品工程技术研究中心重庆市生物制药工程技术研究中心重庆400038

目的分析mir-222在胃癌中的表达水平并鉴定mir-222的靶基因。方法选取第三军医大学新桥医院普外科10例患者的胃癌及远癌组织,匀浆法提取总RNA,用Real-time PCR法检测mir-222表达。利用mirNA靶基因预测数据库TargetScan,MICROCOSM及PicTa... 详细信息

目的分析mir-222在胃癌中的表达水平并鉴定mir-222的靶基因。方法选取第三军医大学新桥医院普外科10例患者的胃癌及远癌组织,匀浆法提取总RNA,用Real-time PCR法检测mir-222表达。利用mirNA靶基因预测数据库TargetScan,MICROCOSM及PicTar对mir-222的靶基因进行预测。化学合成包含有mir-222结合位点的靶基因3′非编码区(3′UTR)退火引物,插入荧光素酶报告载体pmir-REPORT及绿色荧光蛋白(GFP)报告载体pmir-GFP-RE-PORT,检测荧光素酶的活性变化及观察GFP表达量,并在蛋白水平用Western blot检测mir-222对靶基因的抑制。结果 mir-222在70%(7/10)的胃癌组织样本中表达上调。生物信息学(TargetScan,MICROCOSM及PicTar 3个mirNA靶基因预测数据库)分析可得在包括人类在内的不同物种中,FOS基因3′UTR区都有mir-222的保守结合种子序列。通过荧光素酶活性检测和GFP抑制试验可得mir-222在mRNA水平可以与FOS基因结合。Western blot结果显示mir-222可以抑制c-fos蛋白表达。结论 mir-222在胃癌样本中表达上调,证明FOS为mir-222的一个靶基因。

关键词： mir-222 FOS 胃癌

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mir-222促进家兔骨骼肌卫星细胞增殖

西南农业学报 2018年第9期31卷 1973-1978页

作者：刘卜玮杨雪毛旭东梁小虎郑天豪何洪炳赖松家四川农业大学畜禽遗传资源发掘与创新利用四川省重点实验室四川成都611130 成都市农林科学院四川成都611130

【目的】旨在证明mir-222可促进家兔骨骼肌卫星细胞增殖。【方法】利用实时荧光定量(RT-qPCR)法检测mir-222在初生新西兰兔各组织中的表达量;利用targetscan、mirbase等生物信息学软件预测mir-222的靶基因;对靶基因进行KEGG通路分析和G... 详细信息

【目的】旨在证明mir-222可促进家兔骨骼肌卫星细胞增殖。【方法】利用实时荧光定量(RT-qPCR)法检测mir-222在初生新西兰兔各组织中的表达量;利用targetscan、mirbase等生物信息学软件预测mir-222的靶基因;对靶基因进行KEGG通路分析和GO分析,进而预测mir-222是否参与调控骨骼肌卫星细胞增殖;体外培养的骨骼肌卫星细胞转染mir-222过表达和抑制表达载体,利用CCK-8实验和EdU染色实验检测72、96和120 h细胞的增殖情况。【结果】mir-222在各组织中差异表达,且在肝脏中的表达量最高,回肠中的表达量最低;预测得到的靶基因富集到MAPK、PI3K-AKT等多个参与骨骼肌卫星细胞增殖的重要信号通路; CCK-8实验和EdU染色鉴定发现,过表达mir-222能促进骨骼肌卫星细胞增殖,mir-222抑制表达抑制骨骼肌卫星增殖。【结论】mir-222能够促进家兔骨骼肌卫星细胞的增殖。

关键词： mir-222 骨骼肌卫星细胞增殖