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Bioengineered miR-328-3p modulates glut1-mediated glucose uptake and metabolism to exert synergistic antiproliferative effects with chemotherapeutics

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Acta Pharmaceutica Sinica B 2020年第1期10卷 159-170页

作者： Wanrong Yi Mei-Juan Tu Zhenzhen Liu Chao Zhang Neelu Batra Ai-Xi Yu Ai-Ming Yu Department of Orthopaedic Trauma and Microsurgery Zhongnan Hospital of Wuhan UniversityWuhan 430072China Department of Biochemistry&Molecular Medicine UC Davis School of MedicineSacramento 95817CAUSA

MicroRNAs(miRNAs or miRs)are small noncoding RNAs derived from genome to control target gene *** we have developed a novel platform permitting high-yield production of bioengineered miRNA agents(BERA).This study is to produce and utilize novel fully-humanized BERA/miR-3’28-3p molecule(hBERA/miR-3’28)to delineate the role of miR-328-3p in controlling nutrient uptake essential for cell *** first demonstrated successful high-level expression of hBERA/miR-328 in bacteria and purification to high degree of homogeneity(>98%).Biologic miR-328-3p prodrug was selectively processed to miR-328-3p to suppress the growth of highly-proliferative human osteosarcoma(OS)*** glucose transporter protein type 1,gene symbol solute carrier family 2 member 1(GUJTHSLC2A1),we identified and verified large neutral amino acid transporter 1,gene symbol solute carrier family 7 member 5(LPAT1/SLC7A5)as a direct target for miR-3’*** reduction of LAT1 protein levels by miR-3’28-3p did not alter homeostasis of amino acids within OS cells,suppression of glut1 led to a significantly lower glucose uptake and decline in intracellular levels of glucose and glycolytic metabolite ***,combination treatment with hBERA/miR-3’28 and cisplatin or doxorubicin exerted a strong synergism in the inhibition of OS cell *** findings support the utility of novel bioengineered RNA molecules and establish an important role of miR-328-3p in the control of nutrient transport and homeostasis behind cancer metabolism.

关键词： Bioengineered RNA MiR-328 LAT1 glut1 Chemosensitivity Cancer

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CYP3A5 unexpectedly regulates glucose metabolism through the AKT-TXNIP-glut1 axis in pancreatic cancer

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Genes & Diseases 2024年第4期11卷 381-399页

作者： Ming Shao Qingfei Pan Haiyan Tan Jing Wu Ha Won Lee Andrew D.Huber William C.Wright Ji-Hoon Cho Jiyang Yu Junmin Peng Taosheng Chen Department of Chemical Biology and Therapeutics St.Jude Children's Research HospitalMemphisTN 38105USA Department of Computational Biology St.Jude Children's Research HospitalMemphisTN 38105USA Center for Proteomics and Metabolomics St.Jude Children's Research HospitalMemphisTN 38105USA Department of Structural Biology St.Jude Children's Research HospitalMemphisTN 38105USA Department of Developmental Neurobiology St.Jude Children's Research HospitalMemphisTN 38105USA

CYP3A5 is a cytochrome P450(CYP)enzyme that metabolizes drugs and contributes to drug resistance in ***,it remains unclear whether CYP3A5 directly influences cancer *** this report,we demonstrate that CYP3A5 regulates glucose metabolism in pancreatic ductal ***-omics analysis showed that CYP3A5 knockdown re-sults in a decrease in various glucose-related metabolites through its effect on glucose trans-port.A mechanistic study revealed that CYP3A5 enriches the glucose transporter glut1 at the plasma membrane by restricting the translation of TXNIP,a negative regulator of ***,CYP3A5-generated reactive oxygen species were proved to be responsible for atten-uating the AKT-4EBP1-TXNIP signaling ***3A5 contributes to cell migration by maintaining high glucose uptake in pancreatic *** together,our results,for the first time,reveal a role of CYP3A5 in glucose metabolism in pancreatic ductal adenocarcinoma and identify a novel mechanism that is a potential therapeutic target.

关键词： Cell migration CYP3A5 Glucose metabolism glut1 Pancreatic cancer TXNIP

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ZBTB7A governs 2-DG-inhibited glycolysis by regulating glut1 in nasopharyngeal carcinoma

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BIOCELL 2022年第12期46卷 2659-2669页

作者： FEI LIU JIAZHANG WEI JIAO LAN YONGLI WANG JIANXIANG YE CHENG SU MINGZHENG MO FENGZHU TANG BING LI MIN LI WEIMING DENG LINSONG YE WENLIN HUANG JINGJIN WENG WEI JIAO SHENHONG QU Research Center of Medical Sciences The People’s Hospital of Guangxi Zhuang Autonomous RegionGuangxi Academy of Medical SciencesNanning530021China Department of Otolaryngology&Head and Neck The People’s Hospital of Guangxi Autonomous RegionGuangxi Academy of Medical SciencesNanning530021China Department of Medical Oncology Guangxi Medical University Cancer HospitalNanning530021China

Our previous studies suggested a potential interaction between the POK erythroid myeloid ontogenic factor ZBTB7A and glucose transporter 1(glut1)in nasopharyngeal carcinoma(NPC).This study was designed to confirm the interaction and further evaluate the precise mechanism by which ZBTB7A and glut1 regulate NPC *** binding sites between ZBTB7A and the promoter of glut1 were predicted by *** expression was measured by quantitative real-time polymerase chain reaction(qPCR),western blotting,and *** activities of key glycolysis enzymes,including hexokinase(HK),pyruvate kinase(PK),lactate dehydrogenase(LDH),and lactate,were detected using specific enzyme-linked immunosorbent assay *** connection between ZBTB7A and glut1 was analyzed by dual-luciferase reporter assay and chromatin *** vitality,proliferation,and tumorigenicity of the cells expressing different levels of ZBTB7A were tested by adding the glycolysis inhibitor 2-deoxy-D-glucose(2-DG),followed by MTT,colorimetric focus forming,and xenograft assays,*** results showed that high expression of glut1 was associated with late-stage *** constructing stably transfected cells with lentiviruses,ZBTB7A was effectively knocked down in 5-8F cells(RNAi-5-8F)and overexpressed in 6-10B cells(ZBTB7A-6-10B).The up-or downregulation of glut1 secondary to ZBTB7A changes was also *** vitality and proliferation of the cells expressing low ZBTB7A were notably blocked by *** cells expressing high ZBTB7A were not very sensitive to *** growth of RNAi-5-8F xenografts was strongly suppressed by *** activities of HK,PK,and LDH were suppressed by 2-DG in the cells expressing low ***-5-8F cells had the lowest 2-DG-induced lactate ***7A directly suppressed the promoter region of glut1 to regulate glut1 ***,ZBTB7A controls the 2-DG-induced inhibition of glycolysis by affecting glut1.

关键词： Nasopharyngeal carcinoma ZBTB7A glut1 Glycolysis 2-DG

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HSP90B1-mediated plasma membrane localization of glut1 promotes radioresistance of glioblastomas

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The Journal of Biomedical Research 2023年第5期37卷 326-339页

作者： Yanhui Li Yuqian Ge Mengjie Zhao Fangshu Ding Xiuxing Wang Zhumei Shi Xin Ge Xiefeng Wang Xu Qian Department of Nutrition and Food Hygiene Center for Global HealthSchool of Public HealthNanjing Medical UniversityNanjingJiangsu 211166China Institute for Brain Tumors Jiangsu Key Lab of Cancer BiomarkersPrevention and TreatmentJiangsu Collaborative Innovation Center for Cancer Personalized MedicineNanjing Medical UniversityNanjingJiangsu 211166China Department of Neuro-Psychiatric Institute the Affiliated Brain Hospital of Nanjing Medical UniversityNanjingJiangsu 210029China National Health Commission Key Laboratory of Antibody Technologies Nanjing Medical UniversityNanjingJiangsu 211166China Department of Cell Biology School of Basic Medical SciencesNanjing Medical UniversityNanjingJiangsu 211166China Department of Neurosurgery the First Affiliated Hospital of Nanjing Medical UniversityNanjingJiangsu 210029China.

Ionizing radiation is a popular and effective treatment option for glioblastoma(GBM).However,resistance to radiation therapy inevitably occurs during *** is urgent to investigate the mechanisms of radioresistance in GBM and to find ways to improve ***,we found that heat shock protein 90 beta family member 1(HSP90B1)was significantly upregulated in radioresistant GBM cell *** importantly,HSP90B1 promoted the localization of glucose transporter type 1,a key rate-limiting factor of glycolysis,on the plasma membrane,which in turn enhanced glycolytic activity and subsequently tumor growth and radioresistance of GBM *** findings imply that targeting HSP90B1 may effectively improve the efficacy of radiotherapy for GBM patients,a potential new approach to the treatment of glioblastoma.

关键词： HSP90B1 glycolysis glut1 glioblastoma radiotherapy

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Progesterone treatment before experimental hypoxia-ischemia enhances the expression of glucose transporter proteins glut1 and glut3 in neonatal rats

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Neuroscience Bulletin 2013年第3期29卷 287-294页

作者： Xinjuan Li Hua Han Ruanling Hou Linyu Wei Guohong Wang Chaokun Li Dongliang Li Department of Physiology and Neurobiology Xinxiang Medical University Department of Ultrasonic Diagnosis Central Hospital of Xinxiang City Henan Key Lab of Biological Psychiatry

Progesterone is an efficient candidate for treating stroke and traumatic brain damage. The current study was designed to investigate the effects of pro gesterone on glucose transporter proteins （glut1 and glut3） during hypoxicischemic injury in a neo natal rat model. We demonstrated strong staining for glut1 in the walls of blood vessels and glut3 im munoreactivity in hippocampal neurons after hypoxia ischemia. Hypoxiaischemia elevated glut1 and glut3 at both the mRNA and protein levels in the hippocampus, and pretreatment with progesterone （8 mg/kg） further enhanced their accumulation until 24 h after hypoxicischemic injury. These results showed that progesterone treatment induced the accumula tion of both glut1 and glut3 transporters, and an energycompensation mechanism may be involved in the neuroprotective effect of progesterone during hy poxicischemic injury after cerebral ischemic attacks.

关键词： hypoxic-ischemic injury progesterone glut1 glut3 stroke

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glut1与Ki-67在结直肠癌中的表达及其与^(18)F-FDG PET/CT SUV_(max)的相关性

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中国医学影像技术 2011年第9期27卷 1855-1858页

作者：李迎辞于丽娟田墨涵王大龙王文志哈尔滨医科大学附属第三医院PET/CT中心黑龙江哈尔滨150081

目的探讨葡萄糖转运蛋白1(glut1)与细胞增殖抗原标记物Ki-67在结直肠癌(CRC)中的表达及其与18F-FDG PET/CT显像最大标准摄取值(SUVmax)的关系。方法对33例经术后病理证实的CRC患者术前进行全身PET/CT检查,记录病灶的SUVmax,用免疫组化... 详细信息

目的探讨葡萄糖转运蛋白1(glut1)与细胞增殖抗原标记物Ki-67在结直肠癌(CRC)中的表达及其与18F-FDG PET/CT显像最大标准摄取值(SUVmax)的关系。方法对33例经术后病理证实的CRC患者术前进行全身PET/CT检查,记录病灶的SUVmax,用免疫组化方法分析glut1、Ki-67表达,并与SUVmax进行对比分析。结果 glut1和Ki-67在CRC中的表达均高于正常组织(t=-4.22、-3.04,P均glut1在CRC中的阳性表达率显著高于正常组织(χ2=18.94,P1.42%)高于中-低分化(1/3,33.33%)和中分化(16/23,69.57%)CRC。CRC的SUVmax与glut1的表达存在相关性(r=0.63,Pglut1的表达水平。

关键词：结直肠肿瘤 18F氟脱氧葡萄糖正电子发射型体层摄影术体层摄影术,X线计算机 glut1 Ki-67

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斑节对虾glut1基因cDNA的克隆与表达分析

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南方水产科学 2019年第2期15卷 72-82页

作者：何鹏江世贵李运东杨其彬姜松杨丽诗黄建华周发林中国水产科学研究院南海水产研究所深圳试验基地广东深圳518121 上海海洋大学水产与生命学院上海201306 中国水产科学研究院南海水产研究所农业农村部南海渔业资源开发利用重点实验室广东广州510300

该研究利用RACE技术克隆获得了斑节对虾(Penaeus monodon) glut1 (glucose transporter type 1)的cDNA全长序列;采用实时荧光定量的方法研究了Pmglut1在斑节对虾幼体发育过程中、各个组织中及低盐胁迫下的差异表达情况。该基因cDNA开放... 详细信息

该研究利用RACE技术克隆获得了斑节对虾(Penaeus monodon) glut1 (glucose transporter type 1)的cDNA全长序列;采用实时荧光定量的方法研究了Pmglut1在斑节对虾幼体发育过程中、各个组织中及低盐胁迫下的差异表达情况。该基因cDNA开放阅读框(ORF)全长1 476 bp,可编码491个氨基酸。检测Pmglut1基因从受精卵至仔虾期发育过程的表达情况,结果显示,Pmglut1在幼体发育各期的表达量有所波动,但总体呈现上升趋势。组织表达分析发现,Pmglut1在鳃组织中的表达量最高,肝胰腺次之,在卵巢中的表达量最低。急性低盐胁迫后,Pmglut1在肝胰腺中的表达水平显著高于对照组(Pglut1可能在斑节对虾幼体发育及机体应对低盐胁迫过程中具有重要作用,这为进一步研究葡萄糖转运蛋白基因在斑节对虾幼体发育调控和耐低盐胁迫应答中的分子机制提供了理论依据。

关键词：斑节对虾 glut1 基因克隆幼体发育低盐胁迫

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甘露糖通过下调glut1抑制结直肠癌发生及增殖

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食品与发酵工业 2020年第10期46卷 53-59页

作者：王浩李海涛江南大学食品学院江苏无锡214122

为探究甘露糖对结直肠肿瘤发生及增殖的影响,并进一步解释作用机制。该文建立原发结直肠肿瘤小鼠模型,发现甘露糖的干预,能够显著降低结直肠肿瘤病灶的发生率以及发展程度;通过细胞实验,发现一定剂量甘露糖可以显著减弱结直肠癌细胞系HC... 详细信息

为探究甘露糖对结直肠肿瘤发生及增殖的影响,并进一步解释作用机制。该文建立原发结直肠肿瘤小鼠模型,发现甘露糖的干预,能够显著降低结直肠肿瘤病灶的发生率以及发展程度;通过细胞实验,发现一定剂量甘露糖可以显著减弱结直肠癌细胞系HCT116及HT29的增殖,且在刺激浓度为25 mmol/L作用48 h后,能够显著降低两者培养液中葡萄糖的消耗量,分别达到(68. 40±3. 43)%及(58. 78±1. 27)%;通过蛋白质印迹法,发现甘露糖可降低这2株细胞系中葡萄糖转运载体蛋白glut1表达,在动物模型的结直肠组织中也得到了一致的结果。结论显示,甘露糖能够在体外干扰结直肠癌细胞葡萄糖摄取及增殖,降低原发结直肠肿瘤小鼠模型的结直肠肿瘤发生率及发展程度,认为此现象与葡萄糖转运载体蛋白glut1表达下调有关。

关键词：甘露糖结直肠肿瘤细胞增殖 glut1

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miRNA-148b-3p调节胎盘滋养细胞glut1表达与ICP子代糖代谢紊乱关系的研究

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四川大学学报（医学版） 2019年第3期50卷 328-333页

作者：景晓琳邢爱耘白怀吴琳四川大学华西第二医院遗传代谢疾病及围生医学实验室出生缺陷与相关妇儿疾病教育部重点实验室成都610041 四川大学华西第二医院妇产科成都610041

目的研究miRNA-148b-3p在妊娠期肝内胆汁淤积症(intrahepatic cholestasis of pregnancy,ICP)孕妇胎盘组织中的表达及对滋养细胞葡萄糖转运蛋白-1(glucose transporter 1,glut1)的调控,探索ICP孕妇子代糖代谢异常的可能机制。方法收集2... 详细信息

目的研究miRNA-148b-3p在妊娠期肝内胆汁淤积症(intrahepatic cholestasis of pregnancy,ICP)孕妇胎盘组织中的表达及对滋养细胞葡萄糖转运蛋白-1(glucose transporter 1,glut1)的调控,探索ICP孕妇子代糖代谢异常的可能机制。方法收集2017年3月至2018年1月于四川大学华西第二医院产科行剖宫分娩的ICP孕妇30例,正常妊娠孕妇30例,分别收集胎盘组织、母血及脐血,提取胎盘组织miRNA,母血及脐血送检生化指标。采用实时荧光定量PCR验证miR-148b-3p在两组胎盘中的表达差异。通过lipofectaine3000脂质体包裹miR-148b-3p inhibitor/mimics转染人滋养细胞HTR-8,实时荧光定量PCR验证转染后细胞中miR-148b-3p的表达水平;Western blot检测转染后细胞中glut1的表达水平。结果 ICP孕妇母血空腹血糖(fasting blood glucose,FPG)及其胎儿脐血胰岛素水平较对照组增高(P148b-3p表达量较对照组下降(P148b-3p inhibitor后,与转染inhibitor control比较,HTR-8细胞中miR-148b-3p的表达水平下降(Pglut1蛋白的表达量升高(P148b-3p mimics后,与转染mimics control比较,HTR-8细胞中miR-148b-3p的表达水平上升(Pglut1蛋白的表达量降低(P148b-3p可能通过对胎盘滋养细胞glut1表达的负向调控参与了ICP子代糖代谢异常的发生。

关键词： ICP miRNA miRNA-148b-3p glut1 实时荧光定量PCR Western blot

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罗氏沼虾glut1基因克隆及其在血糖稳态调节中的功能

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中国水产科学 2023年第4期30卷 415-424页

作者：许文静丁千千高炜峰敖士齐朱玉洁高晓建张晓君姜群扬州大学动物科学与技术学院

为了探究葡萄糖转运蛋白1 (glucose transporter type 1, glut1)在罗氏沼虾(Macrobrachium rosenbergii)糖代谢调控中的作用,本研究采用cDNA末端快速扩增技术(rapid amplification of cDNA ends,RACE)克隆获得罗氏沼虾Mr-glut1基因全长cDNA序列,该基因全长1929 bp,开放阅读框(open reading frame, ORF) 1446 bp,编码481个氨基酸,分子量为52035.73,等电点为6.76。多序列比对及系统进化树分析结果显示,十足目glut1基因具有较高同源性,均存在12个跨膜结构域,罗氏沼虾glut1与对虾首先聚为一支,表明亲缘关系最近。实时荧光定量PCR结果显示,Mr-glut1在罗氏沼虾各组织均有表达,肠道表达量最高。葡萄糖注射后,罗氏沼虾血淋巴葡萄糖水平、肝糖原和肌糖原含量迅速升高,肠道、肝胰腺和肌肉组织Mr-glut1基因表达显著上调,但Mr-glut1基因表达变化时间延迟于葡萄糖含量的变化。RNA干扰沉默罗氏沼虾体内Mr-glut1基因表达后,血淋巴中葡萄糖和海藻糖含量显著上升。研究表明, Mr-glut1基因可能参与罗氏沼虾血糖稳态调节,在葡萄糖和海藻糖转运过程中发挥重要作用。

关键词：罗氏沼虾 glut1 基因克隆糖代谢 RNA干扰

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