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The E3 ubiquitin ligase HUWE1 acts through the n-myc-DLL1-nOTCH1 signaling axis to suppress glioblastoma progression

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Cancer Communications 2022年第9期42卷 868-886页

作者： Ye Yuan Li-Hong Wang Xian-Xian Zhao Jiao Wang Meng-Si Zhang Qing-Hua Ma Sen Wei Ze-Xuan Yan Yue Cheng Xiao-Qing Chen Hong-Bo Zou Jia Ge Yan Wang Xia Zhang You-Hong Cui Tao Luo Xiu-Wu Bian Institute of Pathology and Southwest Cancer Center Southwest HospitalThird Military Medical University(Army Medical University)and Key Laboratory of Tumor ImmunopathologyMinistry of Education of ChinaChongqing 400038P.R.China Bio-Bank of Southwest Hospital Third Military Medical University(Army Medical University)Chongqing 400038P.R.China Department of Clinical Laboratory Southwest HospitalThird Military Medical University(Army Medical University)Chongqing 400038P.R.China Department of Oncology the Third Affiliated Hospital of Chongqing Medical UniversityChongqing 401120P.R.China

Background:Elucidation of the post-transcriptional modification has led to novel strategies to treat intractable tumors,especially glioblastoma(GBM).The ubiquitin-proteasome system(UPS)mediates a reversible,stringent and stepwise post-translational modification which is closely associated with malignant processes of GBM.To this end,developing novel therapeutic approaches to target the UPS may contribute to the treatment of this disease.This study aimed to screen the vital and aberrantly regulated component of the UPS in GBM.Based on the molecular identification,functional characterization,and mechanism investigation,we sought to elaborate a novel therapeutic strategy to target this vital factor to combat GBM.Methods:We combined glioma datasets and human patient samples to screen and identify aberrantly regulated E3 ubiquitin ligase.Multidimensional database analysis and molecular and functional experiments in vivo and in vitro were used to evaluate the roles of HECT,UBA and WWE domain-containing E3 ubiquitin ligase 1(HUWE1)in GBM.dCas9 synergistic activation mediator system and recombinant adeno-associated virus(rAAV)were used to endogenously overexpress full-length HUWE1 in vitro and in glioma orthotopic xenografts.Results:Low expression of HUWE1 was closely associated with worse prognosis of GBM patients.The ubiquitination and subsequent degradation of n-myc mediated by HUWE1,leading to the inactivation of downstream Delta-like 1(DLL1)-nOTCH1 signaling pathways,inhibited the proliferation,invasion,and migration of GBM cells in vitro and in vivo.A rAAV dual-vector system for packaging and delivery of dCas9-VP64 was used to augment endogenous HUWE1 expression in vivo and showed an antitumor activity in glioma orthotopic xenografts.Conclusions:The E3 ubiquitin ligase HUWE1 acts through the n-myc-DLL1-nOTCH1 signaling axis to suppress GBM progression.Antitumor activity of rAAV dual-vector delivering dCas9-HUWE1 system uncovers a promising therapeutic strategy for GBM.

关键词： DLL1 E3 ubiquitin ligase glioblastoma HUWE1 n-myc nOTCH1 recombinant adenoassociated virus ubiquitin-proteasome system

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TMEM97蛋白对神经母细胞瘤侵袭迁移的影响及机制研究

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中华小儿外科杂志 2022年第12期43卷 1067-1074页

作者：庹文彬向贇蔡秦真陈浩朱红敏沈芯王军宋能袁纯辉华中科技大学同济医学院附属武汉儿童医院检验部武汉430016 武汉大学中南医院病理科武汉430071 华中科技大学同济医学院附属武汉儿童医院神经内科武汉430016 湖北省中西医结合医院检验科武汉430021

目的探究跨膜蛋白(TMEM97蛋白)对神经母细胞瘤(neuroblastoma,nB)转移的影响及潜在作用机制。方法从GEO和TARGET数据库中下载nB的基因测序数据,分析TMEM97与预后的关联性。免疫组织化学检测患儿nB组织和对照组织中TMEM97的蛋白表达。共... 详细信息

目的探究跨膜蛋白(TMEM97蛋白)对神经母细胞瘤(neuroblastoma,nB)转移的影响及潜在作用机制。方法从GEO和TARGET数据库中下载nB的基因测序数据,分析TMEM97与预后的关联性。免疫组织化学检测患儿nB组织和对照组织中TMEM97的蛋白表达。共表达基因富集分析预测TMEM97生物学作用,并在nB细胞株SH-SY5Y中干扰或过表达TMEM97,Transwell和细胞划痕实验检测细胞迁移和侵袭的变化,Western blot检测转移相关蛋白表达水平。分析预测TMEM97与mycn扩增的关联性并结合荧光素酶实验检测n-myc对TMEM97转录的影响。结果TMEM97 mRnA在高危型nB中的表达量显著高于低危型,并与nB患儿总生存率、无病生存率呈负相关。TMEM97蛋白表达水平在nB组织中显著高于对照组织。TMEM97主要与细胞黏附相关,可显著促进nB细胞的侵袭和迁移能力,伴随有LMO1、GPC2、Syntenin-1和MMP9转移相关蛋白的显著上调。在mycn扩增组织中TMEM97 mRnA表达显著高于无扩增组织,并且n-myc可以直接靶向结合启动子促进TMEM97转录,干扰TMEM97的表达可显著抑制n-myc对侵袭和迁移的促进作用。结论TMEM97是一个不良预后因素,受转录因子n-myc直接激活转录并介导nB细胞侵袭和迁移的发生。

关键词：神经母细胞瘤跨膜蛋白 TMEM97 转移 n-myc

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nDRG2 gene copy number is not altered in colorectal carcinoma

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World Journal of Clinical Oncology 2017年第1期8卷 67-74页

作者： Anders Lorentzen Cathy Mitchelmore Eucaryotic Cell Biology Department of Science and Environment Roskilde University

AIM To investigate if the down-regulation of n-myc Downstream Regulated Gene 2(nDRG2) expression in colorectal carcinoma(CRC) is due to loss of the nDRG2 allele(s).METHODS The following were investigated in the human colorectal cancer cell lines DLD-1, Lo Vo and SW-480: nDRG2 mRnA expression levels using quantitative reverse transcriptionpolymerase chain reaction(qRT-PCR); interaction of the myc gene-regulatory protein with the nDRG2 promoter using chromatin immunoprecipitation; and nDRG2 promoter methylation using bisulfite sequencing.Furthermore, we performed qPCR to analyse the copy numbers of nDRG2 and myc genes in the above three cell lines, 8 normal colorectal tissue samples and 40 CRC tissue samples.RESULTS As expected, nDRG2 mRnA levels were low in the three colorectal cancer cell lines, compared to normal colon.Endogenous myc protein interacted with the nDRG2 core promoter in all three cell lines.In addition, the nDRG2 promoter was heavily methylated in these cell lines, suggesting an epigenetic regulatory mechanism.Unaltered gene copy numbers of nDRG2 were observed in the three cell lines.In the colorectal tissues, one normal and three CRC samples showed partial or complete loss of one nDRG2 allele.In contrast, the myc gene was amplified in one cell line and in more than 40% of the CRC cases.COnCLUSIOn Our study suggests that the reduction in nDRG2 expression observed in CRC is due to transcriptional repression by myc and promoter methylation, and is not due to allelic loss.

关键词： n-myc downstream-regulated gene 2 Colorectal carcinoma myc Tumor suppressor Allelic loss Gene amplification Copy number

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DOWn－REGULATIOn　OF　C－myc　OnCOGEnE　DURInG　nGF－InDUCED　DIFFEREnTIATIOn　OF　nEUROBLASTOMA　CELL　LInES

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Chinese Medical Sciences Journal 1994年第3期9卷 152-156页

作者：陈杰刘彤华 AlonzoHRoss DepartmentofPathology PekingUnionMedicalCollegeHospitalCAMS＆PUMCBeijing100730 WorconterFoundationforExperirnerntalBiologyMA01545 USA

ＤＯＷＮ－ＲＥＧＵＬＡＴＩＯＮＯＦＣ－ＭＹＣＯＮＣＯＧＥＮＥＤＵＲＩＮＧＮＧＦ－ＩＮＤＵＣＥＤＤＩＦＦＥＲＥＮＴＩＡＴＩＯＮＯＦＮＥＵＲＯＢＬＡＳＴＯＭＡＣＥＬＬＬＩＮＥＳＣｈｅｎＪｉｅ（陈杰），ＬｉｕＴｏｎｇｈｕａ... 详细信息

ＤＯＷＮ－ＲＥＧＵＬＡＴＩＯＮＯＦＣ－ＭＹＣＯＮＣＯＧＥＮＥＤＵＲＩＮＧＮＧＦ－ＩＮＤＵＣＥＤＤＩＦＦＥＲＥＮＴＩＡＴＩＯＮＯＦＮＥＵＲＯＢＬＡＳＴＯＭＡＣＥＬＬＬＩＮＥＳＣｈｅｎＪｉｅ（陈杰），ＬｉｕＴｏｎｇｈｕａ（刘彤华）ａｎｄＡｌｏｎｚｏＨＲｏ...

关键词：致癌基因 C-myc 神经生长因子神经细胞瘤肿瘤细胞 n-myc

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THE RELATIOnSHIP BETWEEn EXPRESSIOnS OF n-myc AnD c-myc OnCOGEnES In nEUROBLASTOMA:An In SITU HYBRIDIZATIOn AnD IMMUnOCYTOCHEMICAL STUDY

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Chinese Medical Sciences Journal 1999年第2期14卷 102-106页

作者：折晓宁陈杰刘彤华张雷李佩娟王德田 DepartmentofPathology PekingUnionMedicalCollegeHospitalNationalLaboratoryofMedicalMolecularBiologyCAMS＆PUMCBeijing100730 DepartmentofPathology BeijingChildren＇sHospitalBeijing100045

ＩＮＴＲＯＤＵＣＴＩＯＮＮｅｕｒｏｂｌａｓｔｏｍａｏｒｉｇｉｎａｔｅｓｆｒｏｍｔｈｅｓｙｍｐａｔｈｏａｄ－ｒｅｎａｌｌｉｎｅａｇｅｏｆｔｈｅｎｅｕｒａｌｃｒｅｓｔａｎｄｉｔｉｓｔｈｅｍｏｓｔｃｏｍｍｏｎｅｘｔｒａ－ｃ... 详细信息

ＩＮＴＲＯＤＵＣＴＩＯＮＮｅｕｒｏｂｌａｓｔｏｍａｏｒｉｇｉｎａｔｅｓｆｒｏｍｔｈｅｓｙｍｐａｔｈｏａｄ－ｒｅｎａｌｌｉｎｅａｇｅｏｆｔｈｅｎｅｕｒａｌｃｒｅｓｔａｎｄｉｔｉｓｔｈｅｍｏｓｔｃｏｍｍｏｎｅｘｔｒａ－ｃｒａｎｉａｌｔｕｍｏｒｏｆｃｈｉｌ...

关键词： n-myc c-myc 相关性致癌基因神经细胞瘤免疫细胞化学

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Anti-fibrotic Effects and Mechanism of Shengmai Injection(生脉注射液)on Human Hepatic Stellate Cells LX-2

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Chinese Journal of Integrative Medicine 2019年第3期25卷 197-202页

作者： ZHAnG Yi MA Li-tian LI Jie QIAO Yu LIU Jun-ye WAnG Jin REn Qin-you HU Jin-tao ZHEnG Jin Department of Traditional Chinese Medicine Tangdu Hospital The Fourth Military Medical University Department of Endocrinology The 986 Hospital of The People's Liberation Army Department of Anatomy and K.K. Leung Brain Research Center The Fourth Military Medical University Student Brigade The Fourth Military Medical University Department of Radiation Medicine The Fourth Military Medical University Department of Immunology The Fourth Military Medical University

Objective: To investigate the effects of Shengmai Injection(生脉注射液, SMI) on the proliferation, apoptosis and n-myc downstream-regulated gene 2(nDRG2, a tumour suppressor gene) expression in varying densities of human hepatic stellate cells LX-2. Methods: LX-2 cells were cultured in vitro. Then, cells were plated in 96-well plates at an approximate density of 2.5×10~4 cells/mL and cultured for 48, 72, 96 or 120 h followed by the application of different concentrations of SMI(0.6, 1.2, 2.4, 4.8 or 6 μL/mL). Cell proliferation was measured after an additional 24 or 48 h using the 3(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay. The effects of SMI on different cell growth states(cultured for 48, 72, 96, or 120 h) were observed by light microscopy at 24 h after treatment. When the cells reached 80% confluence, apoptosis was detected by flow cytometry after 24 h. Lastly, LX-2 cells were treated with different concentrations of SMI and extracted with protein lysis buffer. The levels of nDRG2 were measured by Western blot. Results: When the LX-2 cells grew for 48, 72, 96 and 120 h, 4.8 and 6 μL/m L of SMI significantly inhibited cell proliferation at 24 and 48 h after treatment(Pnd 2.4 μL/mL of SMI also inhibited cell proliferation at 24 h after treatment when cell growth for 48 h(Pnd at 48 h after treatment when cell growth for 72, 96 and 120 h(PnDRG2 expression level in the LX-2 cell was significantly increased when treated with SMI at concentrations of 1.2, 2.4, 4.8 or 6 μL/mL(Pnclusions: The inhibitory effects of SMI on the proliferation of LX-2 cells were related to not only concentration dependent but also cell density. In addition, SMI(2.4, 4.8 and 6 μL/mL) could accelerate apoptosis in LX-2 cells, and the mechanism might be associated with nDRG2 over-expression.

关键词： Shengmai injection liver fibrosis n-myc downstream-regulated gene 2 LX-2 cell proliferation apoptosis Chinese medicine

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n-myc在造血和血液肿瘤中的作用机制研究进展

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中国实验血液学杂志 2013年第2期21卷 503-507页

作者：沈莉菁曹兰芳陈芳源上海交通大学医学院附属仁济医院血液科上海200127 上海交通大学医学院附属仁济医院儿科上海200127

n-myc癌基因在胚胎期造血细胞增殖、分化过程中起着重要作用。一旦机体发生血液恶性肿瘤时,其表达量可升高,并与不良预后显著相关。本文就n-myc的结构,对各系造血细胞的调控机制,参与各信号通路的交互作用,国内、外的过表达造模研究、... 详细信息

n-myc癌基因在胚胎期造血细胞增殖、分化过程中起着重要作用。一旦机体发生血液恶性肿瘤时,其表达量可升高,并与不良预后显著相关。本文就n-myc的结构,对各系造血细胞的调控机制,参与各信号通路的交互作用,国内、外的过表达造模研究、药物干预等方面的研究进展作一综述。

关键词： n-myc 癌基因造血系统血液肿瘤

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nDRG1在肿瘤侵袭转移相关分子机制中的研究进展

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中华病理学杂志 2018年第1期47卷 75-78页

作者：何易晓朱宇杨丽娟王芳昆明医科大学病理学教研室 650500 河南郑州应用技术职业学院

n-myc 下游调节基因（n-myc down-stream-regulated-gene,nDRG）1是 nDRG 家族成员,人源 nDRG 基因包括nDRG1、nDRG2、nDRG3和nDRG4[1].nDRG家族属于α/β水解酶超家族,但无水解酶催化位点.研究表明,nDRG1与细胞的生长[2]及凋亡[3]、肿瘤细胞增殖[4-5]、缺氧应激反应[6]、肿瘤细胞的药物反应和耐药性[7]、肿瘤侵袭和转移[8]等有关,还能被多种诱导分化剂诱导表达,

关键词：肿瘤侵袭转移 nDRG1 分子机制肿瘤细胞增殖 α/β水解酶调节基因家族成员 n-myc

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n-myc Inhibition: Advances in neuroblastoma Treatment

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CellBio 2017年第3期6卷 27-34页

作者： Md Kamrul Hasan Moores Cancer Center University of California San Diego Health Sciences Dr La Jolla CA USA

neuroblastoma (nBL) is one of the most common solid tumors and around 15% of cancer mortality in children. Amplification of the n-myc proto-oncogene is strongly correlated with advanced disease and poor clinical outcome in nBL. Recent studies described that ubiquitin-specific protease 7 (USP7;also known as HAUSP) interacts with n-myc, induces deubiquitination and subsequent stabilization of n-myc that in-turn potentiates n-myc function, and treatment with the HAUSP inhibitor (P22077) blocked such effects.

关键词： neuroblastoma n-myc PI3K/mTOR PARP1 PD-L1 HAUSP

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间变性大细胞淋巴瘤激酶蛋白在儿童外周神经母细胞性肿瘤中的表达及意义

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实用癌症杂志 2022年第5期37卷 755-757页

作者：陈干樊金星黄慧徐锦杨文萍陶强南昌大学医学院 330006 江西省儿童医院 330006

目的探讨间变性大细胞淋巴瘤激酶蛋白(ALK)在外周神经母细胞性肿瘤(pnT)中的表达及意义。方法收集46例pnT的临床病理资料,采用免疫组化方法检测ALK蛋白,荧光原位杂交技术检测n-myc基因。结果46例患儿临床分期:Ⅰ~Ⅱ期和Ⅲ~Ⅳ期各23例;... 详细信息

目的探讨间变性大细胞淋巴瘤激酶蛋白(ALK)在外周神经母细胞性肿瘤(pnT)中的表达及意义。方法收集46例pnT的临床病理资料,采用免疫组化方法检测ALK蛋白,荧光原位杂交技术检测n-myc基因。结果46例患儿临床分期:Ⅰ~Ⅱ期和Ⅲ~Ⅳ期各23例;病理诊断:神经母细胞瘤(nB)40例、节细胞性神经母细胞瘤(GnB)6例,其中预后良好型(FH型)32例、预后不良型(UH型)14例;ALK在nB和GnB中的阳性表达率分别为55%(22/40)和0(0/6),差异具有统计学意义(P=0.038)。40例nB中n-myc基因扩增阳性4例、获得7例,6例GnB均无n-myc基因扩增和获得。15例新生儿nB中ALK蛋白阳性表达率为40%(6/15),100%n-myc基因扩增阴性。ALK蛋白在Ⅲ~Ⅳ期、UH型和n-myc基因异常中表达率高,差异具有统计学意义(P=0.018、0.001、0.010),在不同性别、年龄和部位间无差异表达(P=0.382、0.400、0.617)。结论儿童pnT应常规检测ALK蛋白,其阳性表达与病理分型和临床分期有一定的关系。不同年龄段nB中ALK蛋白的表达意义及机制有待进一步研究。

关键词：神经母细胞瘤间变性大细胞淋巴瘤 ALK 蛋白儿童新生儿 n-myc 基因

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