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Establishment of xenografts of urological cancers on chicken chorioallantoic membrane(CAM)to study metastasis

Precision Clinical Medicine 2019年第3期2卷 140-151页

作者： Junhui Hu Moe Ishihara Arnold IChin lily wu Department of Molecular and Medical Pharmacology David Geffen School of MedicineUniversity of California at Los AngelesCA 90095USA Department of Urology David Geffen School of MedicineUniversity of California at Los AngelesCA 90095USA Department of Pediatrics David Geffen School of MedicineUniversity of California at Los AngelesCA 90095USA Jonsson Comprehensive Cancer Center David Geffen School of MedicineUniversity of California at Los AngelesCA 90095USA

Cancer of the urological system commonly occurs in the kidney,bladder,and prostate gland.The clear cell subtype of renal cell carcinoma(ccRCC)constitutes the great majority of kidney cancer.Metastatic ccRCC portends a very poor outcome with no effective treatment available.Prostate cancer is the most common cancer in males in the US.Despite recent advances in selective kinase inhibitors and immunotherapies,the rate of developing new treatment from bench to bedside is slow.A time-consuming step is at the animal drug testing stage,in which the mouse model is the gold standard.In the pursuit to streamline the in vivo cancer biology research and drug development,we explored the feasibility of the chicken chorioallantoic membrane(CAM)model to establish xenografts.The CAM model greatly shortens the time of tumor growth and lowers the cost comparing to immunocompromised mice.We generated CAM xenografts from ccRCC,bladder and prostate cancer,with established cancer cell lines and freshly isolated patient-derived tissues,either as primary tumor cells or small pieces of tumors.The successful CAM engraftment rate from the different tumor sources is 70%or above.Using our previously established metastatic ccRCC mouse model,we showed that the CAM xenograft maintains the same tumor growth pattern and metastatic behavior as observed in mice.Taken together,CAM can serve as a valuable platform to establish new patient-derived xenografts(PDXs)to study tumor biology,thus accelerating the development of individualized treatment to halt the deadly metastatic stage of cancer.

关键词： chorioallantoic membrane prostate cancer bladder cancer kidney cancer animal mode

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Enhanced structural stability of adenovirus nanocapsule

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Progress in Natural Science:Materials International 2014年第2期24卷 171-174页

作者： Ding Weng Ziyue Karen Jiang Jing Jin lily wu Yunfeng Lu Chemical and Biomolecular Engineering University of California at Los Angeles Tissue Engineering Laboratories VA Boston Healthcare System Department of Orthopaedic Surgery Brigham and Women's Hospital Harvard Medical School Molecular and Medical Pharmacology University of California at Los Angeles Getein Biotechnology Co. Ltd.

Application of viral vector in gene therapy and vaccination is still limited by their structural stability, which significantly increased avoidable cost in storage and transportation. Herein a non-covalent conjugated low-pH degradable nanocapsule has been adopted to stabilize viral vectors. By utilizing a luciferase expressing adenovirus, AdCMVLuc, we succeeded in a raise of over 11 folds in AdCMVLuc’s structural stability after 12 days storage at 4 1℃.

关键词： Non-covalent nanocapsule Adenovirus Structural stability

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Tumor heterogeneity in VHL drives metastasis in clear cell renal cell carcinoma

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Signal Transduction and Targeted Therapy 2023年第5期8卷 2329-2344页

作者： Junhui Hu Ping Tan Moe Ishihara Nicholas ABayley Shiruyeh Schokrpur Jeremy GReynoso Yangjun Zhang Raymond JLim Camelia Dumitras Lu Yang Steven MDubinett Parmjit SJat Jacques Van Snick Jiaoti Huang Arnold IChin Robert MPrins Thomas GGraeber Hua Xu lily wu Department of Molecular and Medical Pharmacology David Geffen School of MedicineUniversity of California Los AngelesLos AngelesCA90095USA Department of Urology West China HospitalChengduChina Department of Hematology and Oncology University of California San DiegoSan DiegoCA92103USA Department of Neurosurgery David Geffen School of MedicineUniversity of California Los AngelesLos AngelesCA90095USA Department of Biological Repositories Department of UrologyZhongnan Hospital of Wuhan UniversityWuhanChina Department of Medicine David Geffen School of MedicineUniversity of California Los AngelesLos AngelesCA90095USA Jonsson Comprehensive Cancer Center David Geffen School of Medicine at UCLAUniversity of California Los AngelesLos AngelesCA90095USA MRC Prion Unit at UCL Institute of Prion Diseases33 Cleveland StreetLondonW1W 7FFUK Ludwig Institute for Cancer Research Ltd BrusselsBelgium Department of Pathology Duke UniversityDurhamNCUSA Department of Urology David Geffen School of MedicineUniversity of California Los AngelesLos AngelesCA90095USA Cancer Precision Diagnosis and Treatment and Translational Medicine Hubei Engineering Research Center WuhanChina

Loss of function of the von Hippel-Lindau(VHL)tumor suppressor gene is a hallmark of clear cell renal cell carcinoma(ccRCC).The importance of heterogeneity in the loss of this tumor suppressor has been under reported.To study the impact of intratumoral VHL heterogeneity observed in human ccRCC,we engineered VHL gene deletion in four RCC models,including a new primary tumor cell line derived from an aggressive metastatic case.The VHL gene-deleted(VHL-KO)cells underwent epithelial-to-mesenchymal transition(EMT)and exhibited increased motility but diminished proliferation and tumorigenicity compared to the parental VHL-expressing(VHL+)cells.Renal tumors with either VHL+or VHL-KO cells alone exhibit minimal metastatic potential.Combined tumors displayed rampant lung metastases,highlighting a novel cooperative metastatic mechanism.The poorly proliferative VHL-KO cells stimulated the proliferation,EMT,and motility of neighboring VHL+cells.Periostin(POSTN),a soluble protein overexpressed and secreted by VHL non-expressing(VHL−)cells,promoted metastasis by enhancing the motility of VHL-WT cells and facilitating tumor cell vascular escape.Genetic deletion or antibody blockade of POSTN dramatically suppressed lung metastases in our preclinical models.This work supports a new strategy to halt the progression of ccRCC by disrupting the critical metastatic crosstalk between heterogeneous cell populations within a tumor.

关键词： VHL metastasis motility

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Regulative role of the CXCL13-CXCR5 axis in the tumor microenvironment

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Precision Clinical Medicine 2018年第1期1卷 49-56页

作者： Ping Tan Ming Shi Li Lai Zhuang Tang Nan Xie Hang Xu Qiang Wei Xiaoyu Zhang Lu Yang lily wu Department of Urology Institute of UrologyWest China HospitalSichuan UniversityChengduSichuan The Center of Anesthesiology and Surgery West China Hospitalsichuan UniversityChengduSichuan Department of Emergency West China HospitalSichuan UniversityChengduSichuan Department of Molecular and Medical Phamacology David Geffen School of MedicineUniversity of CaliforniaLos AngelesCA 90095USA Department of Urology David Geffen School of MedicineUniversity of CaliforniaLos AngelesCA 90095USA

Chemokines are best known for their abilities of recruiting immune cells and forming lymphoid tissue.Through interactions between chemokines and their receptors,various immune cell subsets are recruited into the tumor microenvironment which is the primary location for tumor cells interacting with responding host cells.In recent decades,a large volume of studies have revealed chemokines'role in the tumor microenviron-ment in regulating tumor growth,invasion,and/or metastasis as well as tumor immune response;however,their molecular mechanisms are not well understood.Recently,increasing evidence has reported the import-ance of the CXCL13-CXCR5 axis in the tumor microenvironment of vanious human malignancies.Thus,in this review,we will focus on the CXCL13-CXCR5 axis and elaborate on the expression patterns,regulating and cor-responding regulatory mechanisms as well as clinical values in a wide range of human cancers.

关键词： chemokine CXCL13 CXCR5 tumor,microenvironment

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Junction plakoglobin regulates and destabilizes HIF2α to inhibit tumorigenesis of renal cell carcinoma

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Cancer Communications 2021年第4期41卷 316-332页

作者： Ke Chen Jin Zeng Yi Sun Wei Ouyang Gan Yu Hui Zhou Yangjun Zhang Weimin Yao Wei Xiao Junhui Hu Jinchun Xing Kefeng Xiao lily wu Zhiqiang Chen Zhangqun Ye Hua Xu Department of Urology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei 430030P.R.China Hubei Institute of Urology WuhanHubei 430030P.R.China Department of Urology The First Affiliated Hospital of Nanchang UniversityNanchangJiangxi 330000P.R.China Department of Molecular and Medical Pharmacology David Geffen School of MedicineUniversity of California at Los AngelesLos AngelesCA 90095USA Department of Urology The First Affiliated Hospital of Xiamen UniversityXiamenFujian 361003P.R.China Department of Urology The People’s Hospital of Shenzhen CityShenzhenGuangdong 518020P.R.China

Background:Increased hypoxia-inducible factor 2α(HIF2α)activation is a common event in clear cell renal cell carcinoma(ccRCC)progression.However,the function and underlying mechanism of HIF2α in ccRCC remains uninvestigated.We conducted this study to access the potential link between junction plakoglobin(JUP)and HIF2αin ccRCC.Methods:Affinity purification and mass spectrometry(AP-MS)screening,glutathione-s-transferase(GST)pull-down and co-immunoprecipitation(Co-IP)assays were performed to detect the interacting proteins of HIF2α.Quantitative PCR(qPCR)and Western blotting were used to detect the expression of JUP in human ccRCC samples.Luciferase reporter assays,chromatin immunoprecipitation(ChIP),cycloheximide chase assays,and ubiquitination assays were conducted to explore the regulation of JUP on the activity of HIF2α.Cell Counting Kit-8(CCK-8)assays,colony formation assays,transwell assays,and xenograft tumor assays were performed to investigate the effect of JUP knockdown or overexpression on the tumorigenicity of renal cancer cells.Results:We identified JUP as a novel HIF2α-binding partner and revealed an important role of JUP in recruiting von Hippel-Lindau(VHL)and histone deacetylases 1/2(HDAC1/2)to HIF2α to regulate its stability and transactivation.JUP knockdown promoted and overexpression suppressed the tumorigenicity of renal cell carcinoma in vitro and in vivo.Importantly,the low expression of JUP was found in clinical ccRCC samples and correlated with enhanced hypoxia scores and poor treatment outcomes.Conclusion:Taken together,these data support a role of JUP in modulating HIF2α signaling during ccRCC progression and identify JUP as a potential therapeutic target.

关键词： renal cell carcinoma junction plakoglobin hypoxia-inducible factor 2α transcriptional activity ubiquitination

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连接桥粒斑珠蛋白通过调节HIF2α并降低其稳定性抑制肾细胞癌的肿瘤发生

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癌症 2022年第1期41卷 18-35页

作者：陈科曾瑾孙旖欧阳为余淦周辉张杨军姚炜敏肖巍胡峻珲邢金春肖克峰 lily wu 陈志强叶章群徐华泌尿外科华中科技大学同济医学院附属同济医院湖北武汉430030 湖北省泌尿外科研究所武汉430030 泌尿外科南昌大学第一附属医院江西南昌330000 分子与医学药理学系戴卫·格芬医学院加州大学洛杉矶分校美国洛杉矶加州90095 泌尿外科厦门大学第一附属医院福建厦门361003 泌尿外科深圳市人民医院广东深圳518020

背景与目的低氧诱导因子(hypoxia-inducible factor 2α,HIF2α)活性增高常见于肾透明细胞癌(clear cell renal cell carcinoma,ccRCC)的进展过程。HIF2α在ccRCC中的功能和作用机制仍不清楚。本研究阐释了连结桥粒斑珠蛋白(junction pl... 详细信息

背景与目的低氧诱导因子(hypoxia-inducible factor 2α,HIF2α)活性增高常见于肾透明细胞癌(clear cell renal cell carcinoma,ccRCC)的进展过程。HIF2α在ccRCC中的功能和作用机制仍不清楚。本研究阐释了连结桥粒斑珠蛋白(junction plakoglobin,JUP)和HIF2α在ccRCC中的作用。方法采用亲和纯化联合质谱(affinity purification and mass spectrometry,AP-MS)、谷胱甘肽-S-转移酶(glutathione-s-transferase,GST)沉降和免疫共沉淀(co-immunoprecipitation,Co-IP)法筛选和鉴定出可与HIF2α相互作用的蛋白质。采用实时荧光定量PCR(quantitative real-time PCR,qPCR)和Western blotting法检测人ccRCC样本中JUP的表达情况。采用荧光素酶报告基因、染色质免疫沉淀(chromatin immunoprecipitation,ChIP)、环己酰亚胺追踪实验、泛素化检测研究JUP对HIF2α活性的调节。采用细胞计数试剂盒-8(Cell Counting Kit-8,CCK-8)检测、集落形成实验、transwell迁移实验、异种移植瘤模型研究JUP敲减或过表达对肾癌细胞致瘤活性的影响。结果我们的研究发现,JUP是一种新的HIF2α结合蛋白,通过将VHL(von Hippel-Lindau,VHL)和组蛋白去乙酰化酶1/2(histone deacetylases 1/2,HDAC1/2)招募到HIF2α并调节其稳定性和转录活性来发挥重要作用。在体内和体外实验中,敲减JUP可促进肾细胞癌的致瘤活性;相反,JUP过表达则可抑制肾细胞癌的致瘤活性。另外,在ccRCC临床样本中JUP低表达,而且其低表达与低氧评分升高及预后更差相关。结论本研究表明JUP在ccRCC进展过程中通过调节HIF2α信号通路发挥重要作用,JUP可作为一个潜在的治疗靶点。

关键词：肾细胞癌连接桥粒斑珠蛋白低氧诱导因子2α 转录活性泛素化

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Cobalt doping amount determines dominant reactive species in peroxymonosulfate activation via porous carbon catalysts co-doped by cobalt and nitrogen

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Journal of Environmental Sciences 2024年第4期138卷 212-226页

作者： Xiang Li Limeng wu Aiqin Zhang Shaohua wu Yan Lin Chunping Yang Key Laboratory of Jiangxi Province for Persistent Pollutants Control and Resources Recycle Nanchang Hangkong UniversityNanchang 330063China Academy of Environmental and Resource Sciences School of Environmental Science and EngineeringGuangdong University of Petrochemical TechnologyMaoming 525000China College of Environmental Science and Engineering Hunan University and Key Laboratory of Environmental Biology and Pollution Control(Hunan University)Ministry of EducationChangsha 410082China

Switching the reaction routes in peroxymonosulfate(PMS)-based advanced oxidation processes have attracted much attention but remain challenging.Herein,a series of Co-N/C catalysts with different compositions and structures were prepared by using bimetallic zeolitic imidazolate frameworks based on ZIF-8 and ZIF-67(x Zn/Co-ZIFs).Results show that Co doping amount could mediate the transformation of the activation pathway of PMS over CoN/C.When Co doping amount was less than 10%,the constructed x Co-N/C/PMS system(x≤10%)was singlet oxygen-dominated reaction;however further increasing Co doping amount would lead to the generation and coexistence of sulfate radicals and high-valent cobalt,besides singlet oxygen.Furthermore,the nitrogen-coordinated Co(Co-NX)sites could serve as main catalytically active sites to generate singlet oxygen.While excess Co doping amount caused the formation of Co nanoparticles from which leached Co ions were responsible for the generation of sulfate radicals and high-valent cobalt.Compared to undoped N/C,Co doping could significantly enhance the catalytic performance.The 0.5%Co-N/C could achieve the optimum degradation(0.488 min^(-1))and mineralization abilities(78.4%)of sulfamethoxazole among the investigated Co-N/C catalysts,which was superior to most of previously reported catalysts.In addition,the application prospects of the two systems in different environmental scenarios(pH,inorganic anions and natural organic matter)were assessed and showed different degradation behaviors.This study provides a strategy to regulate the reactive species in PMS-based advanced oxidation process.

关键词： Peroxymonosulfate Sulfate radical Singlet oxygen Cobalt Zeolitic imidazolate framework Advanced oxidation process

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The physiological role of the unfolded protein response in the nervous system

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Neural Regeneration Research 2024年第11期19卷 2411-2420页

作者： Shuangchan wu Wensheng Lin Department of Neuroscience University of MinnesotaMinneapolisMNUSA Institute for Translational Neuroscience University of MinnesotaMinneapolisMNUSA

The unfolded protein response(UPR)is a cellular stress response pathway activated when the endoplasmic reticulum,a crucial organelle for protein folding and modification,encounters an accumulation of unfolded or misfolded proteins.The UPR aims to restore endoplasmic reticulum homeostasis by enhancing protein folding capacity,reducing protein biosynthesis,and promoting protein degradation.It also plays a pivotal role in coordinating signaling cascades to determine cell fate and function in response to endoplasmic reticulum stress.Recent research has highlighted the significance of the UPR not only in maintaining endoplasmic reticulum homeostasis but also in influencing various physiological processes in the nervous system.Here,we provide an overview of recent findings that underscore the UPR’s involvement in preserving the function and viability of neuronal and myelinating cells under physiological conditions,and highlight the critical role of the UPR in brain development,memory storage,retinal cone development,myelination,and maintenance of myelin thickness.

关键词： myelin neuron oligodendrocyte Schwann cell unfolded protein response

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LONP1 ameliorates liver injury and improves gluconeogenesis dysfunction in acute-on-chronic liver failure

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Chinese Medical Journal 2024年第2期137卷 190-199页

作者： Muchen wu Jing wu Kai Liu Minjie Jiang Fang Xie Xuehong Yin Jushan wu Qinghua Meng Department of Liver Disease Beijing You-An HospitalCapital Medical UniversityBeijing 100069China Beijing Institute of Hepatology Beijing You-An HospitalCapital Medical UniversityBeijing 100069China Department of General Surgery Beijing You-An HospitalCapital Medical UniversityBeijing 100069China

Background:Acute-on-chronic liver failure(ACLF)is a severe liver disease with complex pathogenesis.Clinical hypoglycemia is common in patients with ACLF and often predicts a worse prognosis.Accumulating evidence suggests that glucose metabolic disturbance,especially gluconeogenesis dysfunction,plays a critical role in the disease progression of ACLF.Lon protease-1(LONP1)is a novel mediator of energy and glucose metabolism.However,whether gluconeogenesis is a potential mechanism through which LONP1 modulates ACLF remains unknown.Methods:In this study,we collected liver tissues from ACLF patients,established an ACLF mouse model with carbon tetrachloride(CCl 4),lipopolysaccharide(LPS),and D-galactose(D-gal),and constructed an in vitro hypoxia and hyperammonemia-triggered hepatocyte injury model.LONP1 overexpression and knockdown adenovirus were used to assess the protective effect of LONP1 on liver injury and gluconeogenesis regulation.Liver histopathology,biochemical index,mitochondrial morphology,cell viability and apoptosis,and the expression and activity of key gluconeogenic enzymes were detected to explore the underlying protective mechanisms of LONP1 in ACLF.Results:We found that LONP1 and the expressions of gluconeogenic enzymes were downregulated in clinical ACLF liver tissues.Furthermore,LONP1 overexpression remarkably attenuated liver injury,which was characterized by improved liver histopathological lesions and decreased serum alanine aminotransferase(ALT)and aspartate aminotransferase(AST)in ACLF mice.Moreover,mitochondrial morphology was improved upon overexpression of LONP1.Meanwhile,the expression and activity of the key gluconeogenic enzymes were restored by LONP1 overexpression.Similarly,the hepatoprotective effect was also observed in the hepatocyte injury model,as evidenced by improved cell viability,reduced cell apoptosis,and improved gluconeogenesis level and activity,while LONP1 knockdown worsened liver injury and gluconeogenesis disorders.Conclusion:We demonstrated that gluconeogenesis dysfunc

关键词： Acute-on-chronic liver failure Lon protease-1 Gluconeogenesis disturbance Mitochondrial dysfunction Metabolism

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Ballistic performances of the hourglass lattice sandwich structures under high-velocity fragments

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Defence Technology（防务技术） 2024年第1期31卷 312-325页

作者： He-xiang wu Jia Qu Lin-zhi wu Key Laboratory of Advanced Ship Materials and Mechanics College of Aerospace and Civil EngineeringHarbin Engineering UniversityHarbin150001China School of Civil Engineering Northeast Forestry UniversityHarbin150040China

In this paper,the numerical simulation method is used to study the ballistic performances of hourglass lattice sandwich structures with the same mass under the vertical incidence of fragments.Attention is paid to elucidating the influences of rod cross-section dimensions,structure height,structure layer,and rod inclination angle on the deformation mode,ballistic performances,and ability to change the ballistic direction of fragments.The results show that the ballistic performances of hourglass lattice sandwich structures are mainly affected by their structural parameters.In this respect,structural parameters optimization of the hourglass lattice sandwich structures enable one to effectively improve their ballistic limit velocity and,consequently,ballistic performances.

关键词： Hourglass lattice sandwich structures Ballistic performances high-velocity Finite element analysis

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