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Systematic pan-cancer analysis reveals OGT and OGA as potential biomarkers for tumor microenvironment and therapeutic responses

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Genes & Diseases 2024年第4期11卷 1-4页

作者： Chunyan Hou Ci Wu Wenge Zhu Huadong Pei Junfeng Ma department of Oncology Lombardi Comprehensive Cancer CenterGeorgetown UniversityWashingtonDC 20007USA department of biochemistry and Molecular Medicine School of Medicine and Health ScienceGeorge Washington UniversityWashingtonDC20052USA

Protein O-linkedβ-N-acetylglucosamine(O-GlcNAc)modification(O-GlcNAcylation)is a unique monosaccharide modification of essential importance in physiology and pathology.1,2 As a highly dynamic process,O-GlcNAcylation is mediated by two paired enzymes:O-GlcNAc transferase(OGT)and O-GlcNAcase(OGA),which add or remove the modification from proteins,respectively.Emerging evidence demonstrates that the aberrant O-GlcNAcylation underlies the initiation,progression,and metastasis of cancer.

关键词： metastasis pathology therapeutic

The intracellular mechanism of alpha-fetoprotein promoting the proliferation of NIH 3T3 cells

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Cell Research 2002年第2期12卷 151-156页

作者： MENG SEN LI, PING FENG LI, FBI YI YANG, SHI PENG HE, Guo GUANG DU, GANG LI1 department of biochemistry and Molecular Biology, 2 department of Biophysics, Health Science Center, Peking University, Beijing 100083, China department of biochemistry and Molecular Biology Health Science Center Peking University Beijing China department of Biophysics Health Science Center Peking University Beijing China

AIM The existence and properties of alpha-fetoprotein (AFP) receptor on the surface of NIH 3T3 cells and the effects of AFP on cellular signal transduction pathway were investigated. METHODS The effect of AFP on the proliferation of NIH 3T3 cells was measured by incorporation of 3H-TdR. Receptor-binding assay of 125I-AFP was performed to detect the properties of AFP receptor in NIH 3T3 cells. The influences of AFP on the [cAMP]i and the activities of protein kinase A (PKA) were determined. Western blot was used to detect the change of K-ras P21 protein expression. RESULTS The proliferation of NIH 3T3 cells treated with 0-80 mg/L of AFP was significantly enhanced. The Scatchard analysis indicated that there were two classes of binding sites with KD of 2.722×10-9M (Bmax=12810 sites per cell) and 8.931× 10-8M (Bmax=119700 sites per cell) respectively. In the presence of AFP (20 mg/L), the content of cAMP and activities of PKA were significantly elevated . The level of K-ras P21 protein was upregulated by

关键词： Alpha-fetoprotein receptor signal transduction monoclonal antibody gene expression.

CMKLR1 senses chemerin/resolvin E1 to control adipose thermogenesis and modulate metabolic homeostasis

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Fundamental Research 2024年第3期4卷 575-588页

作者： Zewei Zhao Siqi Liu Bingxiu Qian Lin Zhou Jianglin Shi Junxi Liu Lin Xu Zhonghan Yang department of biochemistry Molecular Cancer Research CenterSchool of MedicineSun Yat-sen UniversityShenzhenGuangdong 518107China department of biochemistry Zhongshan School of MedicineSun Yat-sen UniversityGuangzhouGuangdong 510080China School of Public Health Sun Yat-sen UniversityGuangzhouGuangdong 510080China

Induction of beige fat for thermogenesis is a potential therapy to improve homeostasis against obesity.β3-adrenoceptor(β3-AR),a type of G protein-coupled receptor(GPCR),is believed to mediate the thermogenesis of brown fat in mice.However,β3-AR has low expression in human adipose tissue,precluding its activation as a standalone clinical modality.This study aimed at identifying a potential GPCR target to induce beige fat.We found that chemerin chemokine-like receptor 1(CMKLR1),one of the novel GPCRs,mediated the development of beige fat via its two ligands,chemerin and resolvin E1(RvE1).The RvE1 levels were decreased in the obese mice,and RvE1 treatment led to a substantial improvement in obese features and augmented beige fat markers.Inversely,despite sharing the same receptor as RvE1,the chemerin levels were increased in obesogenic conditions,and chemerin treatment led to an augmented obese phenotype and a decline of beige fat markers.Moreover,RvE1 and chemerin induced or restrained the development of beige fat,respectively,via the mechanistic target of rapamycin complex 1(mTORC1)signaling pathway.We further showed that RvE1 and chemerin regulated mTORC1 signaling differentially by forming hydrogen bonds with different binding sites of CMKLR1.In conclusion,our study showed that RvE1 and chemerin affected metabolic homeostasis differentially,suggesting that selectively modulating CMKLR1 may be a potential therapeutic target for restoring metabolic homeostasis.

关键词： Obesity Insulin resistance Thermogenesis CMKLR1 Resolvin E1 Chemerin

Bis(7)-Tacrine, a Promising Anti-Alzheimer's Agent,Attenuates Glutamate-Induced Cell Injury in Primary Cultured Cerebrocortical Neurons of Rats

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Wuhan University Journal of Natural Sciences 2001年第3期6卷 737-741页

作者： Zhang Bai fang,Peng Fang fang,Zhang Jiang zhou,Wu Dong cheng  biochemistry department, School of Medicine, Wuhan University, Wuhan 430071, China biochemistry department School of Medicine Wuhan University Wuhan China

The effects of bis(7) tacrine, a novel dimeric acetylcholinesterase (AChE) inhibitor, on glutamate induced cell injury were investigated in primary cerebral cortical neurons of rats. Exposure of cultured neurons (12 days after plating) to 0.5 mmol/L glutamate for 30 min resulted in significant cell damage. Pretreatment with bis(7) tacrine (0.03 1.0 μmol/L) reduced the glutamate induced neurotoxicity in a concentration dependent manner and the maximal response was seen at 1 μmol/L with approximately 30% protection. A receptor binding assay showed that bis(7) tacrine can completely displace MK 801 binding to rat cortical membrane with an IC 50 of 0.57 μmol/L. These findings suggest that bis(7) tacrine can directly interact with N methyl D aspartate receptor channel complex, which may contribute to the inhibitor's protective effects against glutamate induced excitotoxicity. Thus, it is possible that anti glutamate/anti AChE synergism is responsible for potentially better Alzheimer's therapy of bis(7) tacrine relative to tacrine.

关键词： bis(7) tacrine tacrine cholinesterase inhibitor glutamate primary neuronal cell culture

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Regulation of EGF-induced ERK/MAPK Activation and EGFR Internalization by G Protein-coupled Receptor Kinase 2

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Acta Biochimica et Biophysica Sinica 2005年第8期37卷 525-531页

作者： Jingxia GAO~(1,2*) Jiali LI~1 Lan MA~(1*) ~1 Pharmacology Research Center,Shanghai Medical College.Fudan University,Shanghai 200032,China ~2 department of biochemistry Medical College,Tongji University,Shanghai 200092,China Pharmacology Research Center Shanghai Medical College Fudan UniversityShanghai 200032 China department of biochemistry Medical College Tongji UniversityShanghai 200092 China

G protein-coupled receptor kinases(GRKs)mediate agonist-induced phosphorylation anddesensitization of various G protein-coupled receptors(GPCRs).We investigate the role of GRK2 on epidermalgrowth factor(EGF)receptor signaling,including EGF-induced extracellular signal-regulated kinase andmitogen-activated protein kinase(ERK/MAPK)activation and EGFR internalization.Immunoprecipitationand immunofluorescence experiments show that EGF stimulates GRK2 binding to EGFR complex and GRK2translocating from cytoplasm to the plasma membrane in human embryonic kidney 293 cells.Westernblotting assay shows that EGF-induced ERK/MAPK phosphorylation increases 1.9-fold,1.1-fold and 1.5-fold(P<0.05)at time point 30,60 and 120 min,respectively when the cells were transfected with GRK2,suggesting the regulatory role of GRK2 on EGF-induced ERK/MAPK activation.Flow cytometry experimentsshow that GRK2 overexpression has no effect on EGF-induced EGFR internalization,however,it increasesagonist-induced G protein-coupled δ opioid receptor internalization by approximately 40% (P<0.01).Overall,these data suggest that GRK2 has a regulatory role in EGF-induced ERK/MAPK activation,and that themechanisms underlying the modulatory role of GRK2 in EGFR and GPCR signaling pathways are somewhatdifferent at least in receptor internalization.

关键词： G protein-coupled receptor kinase receptor tyrosine kinase epidermal growth factor receptor ERK/MAPK internalization

Human Acyl-CoA:cholesterol Acyltransferase (ACAT) and its Potential as a Target for Pharmaceutical Intervention against Atherosclerosis

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Acta Biochimica et Biophysica Sinica 2006年第3期38卷 151-156页

作者： Catherine CHANG Ruhong DONG Akira MIYAZAKI Naomi SAKASHITASecond department of Pathology,Kumamoto University School of Medicine,Kumamoto,Japan Jay LIU Michael GUO department of biochemistry Dartmouth Medical School Hanover New Hampshire 03755 USA Showa University School of Medicine Tokyo Japan

Acyl-CoA:cholesterol acyltransferase (ACAT) catalyzes the formation of cholesteryl estersfrom cholesterol and long-chain fatty-acyl-coenzyme A.At the single-cell level,ACAT serves as a regulatorof intracellular cholesterol homeostasis.In addition,ACAT supplies cholesteryl esters for lipoproteinassembly in the liver and small intestine.Under pathological conditions,the accumulation of cholesterylesters produced by ACAT in macrophages contributes to foam cell formation,a hallmark of the earlystage of atherosclerosis.Several reviews addressing various aspects of ACAT and ACAT inhibitors areavailable [1-8].This review briefly outlines the current knowledge on the biochemical properties of humanACATs,and then focuses on discussing the merit of ACAT as a drug target for pharmaceutical interventionsagainst atherosclerosis.

关键词： acyl-CoA cholesterol acyltransferase cholesterol cholesteryl ester atherosclerosis

Trimethylamine N-oxide generation process was influenced by the proportion and source of macronutrients in the diet

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Food Science and Human Wellness 2024年第2期13卷 649-658页

作者： Chengcheng Wang Xuefeng Duan Xiaoyue Li Jinyue Yang Changhu Xue Teruyoshi Yanagita Tiantian Zhang Yuming Wang College of Food Science and Engineering Ocean University of ChinaQingdao 266003China Laboratory for Marine Drugs and Bioproducts Pilot National Laboratory for Marine Science and Technology(Qingdao)Qingdao 266237China Laboratory of Nutrition biochemistry Department of Applied Biochemistry and Food ScienceSaga UniversitySaga 840-8502Japan

Trimethylamine N-oxide(TMAO)is a risk factor of various chronic diseases,which was produced by metabolism from precursors to trimethylamine(TMA)in gut and the oxidation from TMA in liver.The TMA generation was influenced by diet,mainly due to the rich TMAO precursors in diet.However,it was still unclear that the effects of different proportion and source of macronutrients in different dietary pattern on the production process of TMAO.Here,the generation of TMA from precursors and TMAO from TMA was determined after single oral choline chloride and intraperitoneal injection TMA,respectively,in mice fed with carbohydrates,proteins and fats in different proportion and sources.The results suggested that the generation of TMAO was increased by low non-meat protein and high fat via enhancing the production of TMAO from TMA,and decreased by plant protein and refined sugar via reducing TMA production from precursors in gut and TMAO transformation from TMA in liver.The high fat and high sugar diets accelerating the development of atherosclerosis did not increase the production of TMAO,the risk factor for atherosclerosis,which indicated that the dietary compositions rather than the elevated TMAO level might be a more key risk factor for atherosclerosis.

关键词： Trimethylamine N-oxide(TMAO) Trimethylamine(TMA) Dietary composition Macronutrients Gut microbiota

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DPY19L3 promotes vasculogenicmimicry by its C-mannosyltransferase activity

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Oncology Research 2024年第4期32卷 607-614页

作者： HASSAN BAYDOUN YUJI KATO HIROKI KAMO ANNA HÜSCH HAYATO MIZUTA RYOTA KAWAHARA SIRO SIMIZU department of Applied Chemistry Faculty of Science and TechnologyKeio UniversityYokohama223-8522Japan department of Pharmacy and biochemistry Faculty of ScienceUniversity of TübingenTübingen72074Germany

C-mannosylation is a post-translational modification that occurs intracellularly in the endoplasmic reticulum.In humans,biosynthesis of C-mannosylation in proteins containing thrombospondin type 1 repeat is catalyzed by the DPY19 family;nonetheless,biological functions of protein C-mannosylation are not yet fully understood,especially in tumor progression.Vasculogenic mimicry(VM)is the formation of fluid-conducting channels by highly invasive and genetically deregulated tumor cells,enabling the tumors to form matrix-embedded vasculogenic structures,containing plasma and blood cells to meet the metabolic demands of rapidly growing tumors.In this study,we focused on DPY19L3,a C-mannosyltransferase,and aimed to unravel its role in VM.Knockout of DPY19L3 inhibited the formation of VM in HT1080 human fibrosarcoma cells.Re-expression of wild-type DPY19L3 recovered VM formation;however,DPY19L3 isoform2,an enzymatic activity-defect mutant,did not restore it,suggesting that the C-mannosyltransferase activity of DPY19L3 is crucial to its function.Furthermore,the knockdown of DPY19L3 in MDA-MB-231 breast cancer cells hindered its network formation ability.Altogether,our findings suggest that DPY19L3 is required for VM formation and stipulate the relevance of C-mannosylation in oncogenesis.

关键词： C-mannosylation Vasculogenic mimicry DPY19L3

Enhancement of human ACAT1 gene expression to promote the macrophage-derived foam cell formation by dexamethasone

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Cell Research 2004年第4期14卷 315-323页

作者： Li YANG, Jin Bo YANG, Jia CHEN, Guang Yao YU, Pei ZHOU, Lei LEI, Zhen Zhen WANG, Catherine CY CHANG, XinYing YANG, Ta Yuan CHANG, Bo Liang LI State Key Laboratory of Molecular Biology, Institute of biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, 320 Yueyang Road Shanghai 200031, China. department of biochemistry, Dartmouth Medical School, Hanover, NH 03756 USA. State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Graduate School of the Chinese Academy of Sciences Shanghai China department of biochemistry Dartmouth Medical School Hanover USA

In macrophages, the accumulation of cholesteryl esters synthesized by the activated acyl-coenzyme A:cholesterol acyltransferase-1 (ACAT1) results in the foam cell formation, a hallmark of early atherosclerotic lesions. In this study, with the treatment of a glucocorticoid hormone dexamethasone (Dex), lipid staining results clearly showed the large accumulation of lipid droplets containing cholesteryl esters in THP-1-derived macrophages exposed to lower concentration of the oxidized low-density lipoprotein (ox-LDL). More notably, when treated together with specific anti-ACAT inhibitors, the abundant cholesteryl ester accumulation was markedly diminished in THP-1-derived macrophages, confirming that ACAT is the key enzyme responsible for intracellular cholesteryl ester synthesis. RT-PCR and Western blot results indicated that Dex caused up-regulation of human ACAT1 expression at both the mRNA and protein levels in THP-1 and THP-1-derived macrophages. The luciferase activity assay demonstrated that Dex coul

关键词： ACAT dexamethasone macrophage cholesteryl ester gene promoter.