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Glycoside hydrolase family 18 and 20 enzymes are novel targets of the traditional medicine berberine

Glycoside hydrolase family 18 and 20 enzymes are novel targe...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Yanwei Duan Tian Liu Yong Zhou Tongyi Dou Qing Yang State Key Laboratory of Fine Chemical Engineering School of Life Science and Biotechnology and School of SoftwareDalian University of Technology School of Life Science and Medicine Dalian University of Technology Institute of Plant Protection Chinese Academy of Agricultural Sciences

Berberine is a traditional medicine that has multiple medicinal and agricultural ***,little is known about whether berberine can be a bioactive molecule toward carbohydrate-active enzymes,which play numerous vital roles in the life *** this study,berberine and its analogs were discovered to be competitive inhibitors of glycoside hydrolase family 20 β-N-acetyl-D-hexosaminidase（GH20 Hex） and GH18 chitinase from both humans and the insect pest Ostrinia *** and its analog SYSU-1 inhibit insect GH20 Hex from ***（Of Hex1）,with Ki values of 12 and 8.5 μM,***-crystallization of berberine and its analog SYSU-1 in complex with Of Hex1 revealed that the positively charged conjugate plane of berberine forms π-π stacking interactions with Trp,which are vital to its inhibitory ***,the 1,3-dioxole group of berberine binds an unexplored pocket formed by Trp,Trp and Val,which also contributes to its inhibitory *** was also found to be an inhibitor of human GH20 Hex（Hs HexB）,human GH18 chitinase（Hs Cht and AMCase） and insect GH18 chitinase（Of ChtI）.Besides GH18 and GH20 enzymes,berberine was shown to weakly inhibit human GH84 O-GlcNAcase（Hs OGA） and Saccharomyces cerevisiae GH63 α-Glucosidase I（Sc Glu I）.By analyzing the published crystal structures,berberine was revealed to bind with its targets in an identical mechanism,namely via π-π stacking and electrostatic interactions with the aromatic and acidic residues in the binding *** paper reports new molecular targets of berberine and may provide a berberine-based scaffold for developing multi-target drugs.

关键词： berberine glycoside hydrolase β-N-acetyl-D-hexosaminidase chitinase inhibitor

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Hepatic stimulator substance resists hepatic ischemia-reperfusion injury by regulating Drp1 translocation and activation

Hepatic stimulator substance resists hepatic ischemia-reperf...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Chao Zhang Jing Huang Wei An Department of Cell Biology and Municipal Laboratory of Liver Protection and Regulation of Regeneration Capital Medical University

Ischemia-reperfusion injury(IRI),induced by abnormal mitochondrial fission related apoptosis,is a major concern in liver transplantation *** previous studies have demonstrated that hepatic stimulator substance(HSS) is an antiapoptotic effector and could protect liver from ***,the underlying mechanism remains *** the present study,we report that in vitro and in vivo HSS could regulate mitochondrial fission and hepatocyte apoptosis during liver IRI by orchestrating the translocation and activation of dynamin-related protein 1(Drp1).Using a mouse model of IR-induced liver injury,we found that HSS haploinsufficient(HSS+/-) mice displayed exacerbated liver damage based on their increased serum aminotransferase levels,cell structural destruction,and apoptosis levels compared to the wild type(HSS+/+) *** of HSS markedly increased cyclin-dependent kinase 1(CDK1) and Bax expression,accompanied with elevated p-Drp1 and release of cytochrome *** parallel in vitro studies,we found that HSS could inhibit the expression of CDK1 and that HSS inhibits hepatocytes apoptosis through its suppression of CDK1/cyclin B-mediated phosphorylation at Ser-616 of Drp1,thereby decreasing Drp1 accumulation in mitochondria and Drp1-mediated activation of the mitochondrial fission *** the contrary,knockdown of HSS increased of CDK1 as well as Drp1 phosphorylation and aggravated hepatocellular *** investigation showed that HSS was able to reduce the stability and translation of CDK1 mRNA by modulating the expression of several miRNAs,including miR-410-3 p,miR-490-3 p and miR-582-5 *** data reveal a novel mechanism for HSS in regulating the mitochondrial fission machinery and further suggest that modulation of HSS may provide a therapeutic approach for combating liver damage.

关键词： Hepatic stimulator substance dynamin-related protein-1 mitochondrial fission apoptosis ischemia-reperfusion injury

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SLC27A5缺失通过激活Keap1/Nrf2通路促进肝癌增殖的机制研究

SLC27A5缺失通过激活Keap1/Nrf2通路促进肝癌增殖的机制研究

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者：高庆祝张桂冀郑亚秋杨翼黄爱龙汪凯唐霓重庆医科大学感染性疾病分子生物学教育部重点实验室

目的研究溶质载体家族27成员5(Solute Carrier Family 27 Member 5,SLC27A5)在肝癌发生发展中的作用及其分子机制。方法利用TCGA数据分析肝癌与癌旁组织中SLC27A5表达情况及其与预后的关系,并在临床肝癌标本中进行Western Blot和免疫组... 详细信息

目的研究溶质载体家族27成员5(Solute Carrier Family 27 Member 5,SLC27A5)在肝癌发生发展中的作用及其分子机制。方法利用TCGA数据分析肝癌与癌旁组织中SLC27A5表达情况及其与预后的关系,并在临床肝癌标本中进行Western Blot和免疫组化验证;利用重组腺病毒和CRISPR/Cas9系统,分别建立SLC27A5过表达和基因敲除两种细胞模型,通过MTS、EdU和克隆形成实验观察SLC27A5对肝癌细胞增殖的影响,通过裸鼠皮下成瘤和肝原位移植瘤模型观察SLC27A5对肿瘤增殖的影响;利用RNA-Seq技术分析SLC27A5调控的靶基因,q-PCR、Western Blot和IHC技术证实SLC27A5对靶基因的调控;利用抗氧化反应元件(Anti-oxidant response element, ARE)-荧光素酶活性报告系统、q-PCR和Western Blot检测Keap1/Nrf2信号通路的活化状态;利用CellROX?Orange探针,丙二醛(MDA)检测试剂盒和4-羟基壬烯酸(4-HNE)抗体分别检测细胞内活性氧(ROS)和脂质过氧化水平;利用超高效液相色谱-串联质谱/质谱法(UPLC-MS/MS)测定4-HNE对Keap1蛋白半胱氨酸残基的修饰;肝癌细胞、裸鼠皮下成瘤和肝原位移植瘤模型中,观察沉默TXNRD1联合索拉菲尼处理对肝癌细胞和肿瘤增殖和凋亡能力的影响。结果 TCGA数据分析和临床肝癌组织检测发现SLC27A5在肝癌组织中显著低表达(p<0.001),其表达与肝细胞癌患者预后呈正相关(p<0.01)。过表达SLC27A5抑制PLC/PRF/5和SK-Hep1细胞增殖;敲除SLC27A5基因促进HepG2细胞增殖,裸鼠皮下成瘤模型中过表达SLC27A5抑制肝癌增殖;肝原位移植瘤模型中敲除SLC27A5促进肝癌增殖。过表达SLC27A5下调TXNRD1表达,敲除SLC27A5上调TXNRD1的表达,临床肝癌组织标本中SLC27A5 mRNA表达与TXNRD1 mRNA表达成负相关(r=-0.35,p=0.02)。过表达SLC27A5抑制ARE荧光素酶活性、Nrf2核转位和下游靶基因表达;敲除SLC27A5增加ARE荧光素酶活性、促进Nrf2核转位和下游靶基因表达。过表达SLC27A5抑制ROS产生和脂质过氧化,敲除SLC27A5促进ROS产生和脂质过氧化。UPLC-MS/MS检测4-HNE修饰Keap1蛋白半胱氨酸残基位点是Cys513和Cys518。与单用索拉非尼相比,沉默TXNRD1联合索拉菲尼明显抑制肝癌细胞和肿瘤增殖、促进肝癌细胞和肿瘤凋亡。结论 SLC27A5异常低表达,增加ROS和脂质过氧化水平,激活Keap1/Nrf2抗氧化信号通路,上调TXNRD1表达,促进肝癌增殖。

关键词： SLC27A5 肝细胞癌 ROS Keap1/Nrf2信号通路 TXNRD1 索拉非尼

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脐带间充质干细胞分泌因子脂质体囊泡制备及对损伤组织修复作用的研究

脐带间充质干细胞分泌因子脂质体囊泡制备及对损伤组织修复作用的...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者：刘美林傅松涛常冰梅山西医科大学生物化学与分子生物学教研室山西省生物医药健康研究生教育创新中心

背景:研究人脐带间充质干细胞条件培养基制备的脂质体对大鼠皮肤烫伤创面愈合的影响。分离纯化和增殖培养脐带间充质干细胞,收集无动物源性干细胞分泌因子制备成脂质体囊泡,观察脂质体的形态与粒径分布,通过细胞学和动物实验观察其对皮... 详细信息

背景:研究人脐带间充质干细胞条件培养基制备的脂质体对大鼠皮肤烫伤创面愈合的影响。分离纯化和增殖培养脐带间充质干细胞,收集无动物源性干细胞分泌因子制备成脂质体囊泡,观察脂质体的形态与粒径分布,通过细胞学和动物实验观察其对皮肤创伤的修复作用和生物安全性,为创伤治疗提供新型干细胞基质制剂并对其作用机理和安全性进行初步的探讨和评估。方法:1.脐带组织贴壁法分离纯化和传代培养hUC-MSC,观察其形态,并对其表面标记物和成脂肪细胞、成骨细胞分化能力进行检测。2.收集无动物源性hUC-MSC分泌因子(条件培养液),通过ELISA法对收集的条件培养基进行VEGF、IL-8、MCP-1因子的定量测定。3.用薄膜分散法制备hUC-MSC因子脂质体囊泡,对其进行电镜下超微形态的观察和粒径分布特征的测定。4.通过动物实验观察hUC-MSC条件培养液及其脂质体对大鼠皮肤缺损模型的创伤修复作用,进一步对其有效性、作用机理和安全性进行探讨和评估。结果:1.光镜下,hUC-MSC呈大小形态均一的长梭型旋涡状,流式细胞仪检测hUC-MSC阳性标志物CD29、CD44、105的表达率均≥95%,阴性标志物CD34、CD45的表达率≤5%,且hUC-MSC可被诱导分化为脂肪细胞和骨细胞。***-MSC条件培养液中含有干细胞分泌因子,在P5代时,蛋白浓度为0.145mg/mL,经考马斯亮蓝染色有蛋白条带出现,经ELISA测定,条件培养液中VEGF、IL-8、MCP-1的浓度分别为558.60 pg/mL、5236.48pg/mL、2972.55pg/mL;而空白培养基中,蛋白含量为0.002 mg/mL,因子VEGF、IL-8、MCP-1的浓度分别为0.000 pg/mL、0.000pg/mL、0.000pg/mL。3.用薄膜分散法制备得到hUC-MSC分泌因子脂质体,其粒径呈拟正态分布,粒径范围在37.84nm～3580.00nm,平均粒径为262.3nm;电镜下,hUC-MSC分泌因子脂质体呈不规则的圆球状,大小不均一,但分散比较均匀。4.大鼠皮肤创口修复实验表明,hUC-MSC条件培养基液和其脂质体制剂均可以促进创伤的修复,创口及周边组织石蜡切片HE染色后,光镜下观察可见:空白对照组与空白脂质体对照组,创面修复缓慢,真皮层及创面深层未见腺体和毛囊生成,有组织水肿;干细胞分泌因子组,早期大鼠皮肤创面有肉芽组织生成,大鼠皮肤表皮层加厚,真皮层创面肉芽组织增加,有大量新生血管,创面下腺体与毛囊增多;hUC-MSC分泌因子脂质体组,早期大鼠皮肤创面有肉芽组织生成,表皮层加厚大鼠皮肤创面肉芽组织增加,有大量新生血管生成,创面下及皮肤深层的腺体与毛囊增多。结论:1.贴壁培养法可获得高纯度且形态均一的hUC-MSC。2.可用无血清的基础培养基获得无动物源性的干细胞分泌因子(条件培养基)。3.干细胞分泌因子及其脂质体囊泡均可促进大鼠皮肤缺损的创伤修复。

关键词：人脐带间充质干细胞干细胞分泌因子脂质体囊泡创伤修复

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碱基和糖环结构改变而形成的DNA损伤导致DNA复制突变的分子机制研究

碱基和糖环结构改变而形成的DNA损伤导致DNA复制突变的分子机制研...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者：张慧东四川大学华西公共卫生学院

外源性环境毒物和内源性物质会形成各种DNA损伤,导致DNA复制突变,造成DNA序列永久改变,产生各种疾病、丧失某些功能、导致畸形甚至死亡。DNA损伤包括碱基结构改变和糖环结构改变的DNA损伤。研究DNA损伤导致DNA复制突变的分子机制为理解... 详细信息

外源性环境毒物和内源性物质会形成各种DNA损伤,导致DNA复制突变,造成DNA序列永久改变,产生各种疾病、丧失某些功能、导致畸形甚至死亡。DNA损伤包括碱基结构改变和糖环结构改变的DNA损伤。研究DNA损伤导致DNA复制突变的分子机制为理解DNA损伤产生各种疾病提供重要的理论指导。我们纯化了酵母菌DNA聚合酶Polη的催化结构域Polηcore(N端1-513氨基酸),可体现出聚合酶通过DNA损伤的本征活性。在正常模板G上的错配率为10-4。在O6-MeG上的错配率为0.05-0.4,67%插入的是dTTP,31%是dCTP,2%是dATP。在脱碱基位上,错配率在0.03-1之间,53%插入的是dGTP,33%是dATP,还有14%会形成-1移码突变,说明遵循了G-,A-和-1移码突变规则。在8-oxoG上,仍然优先插入dCTP,占57%,其余的是dATP。这些损伤都在不同程度上阻碍了DNA的复制过程。这些研究为深入理解酵母菌DNA聚合酶在通过DNA损伤的分子机制提供了重要理论指导(Mutat Res-Fund Mol M, 779, 134-143, 2015;Biochimie, 121:161-169, 2016;Mutat Res Rev, 768:53-67,2016;Arch Biochem Biophys, 596:99-107, 2016)。我们又研究铜绿假单胞菌噬菌体PaP1的DNA聚合酶gp90,是A-类聚合酶,具有高延伸性和3’-5’外切酶活性。采用消除了外切酶活性的gp90 exo-,发现8-oxoG和O6-MeG可部分抑制gp90 exo-的延伸能力。正常模板G上的错配率在10-4-10-5之间。对于8-oxoG,dNTP插入效率降低,但错配率不变。对于O6-MeG,更倾向于插入错误的dTTP,比dCTP插入效率高出67倍。在8-oxoG对位插入dCTP和dATP以及在O6-MeG的对位插入dCTP和dTTP都产生快速相。存在dNTP和Mg2+时,8-oxoG和O6-MeG损伤都会削弱聚合酶与DNA的结合。脱碱基位阻断了gp90的DNA复制,dATP优先插入到脱碱基位对位,遵循A-rule,与5端的模板序列无关。DNA中的脱碱基位削弱了聚合酶和DNA之间的结合亲和性,然而dNTP的种类并不影响这些结合亲和性。这些研究为深入理解PaP1的DNA聚合酶功能及其在跨损伤DNA合成中的分子机制提供了重要的基础(Virus Genes, 52:538-51, 2016;Genes, 2017, 8, 1 (invited);DNA Repair, 57, 35-44, 2017;Chem. Res. Toxicol., 31:58-65, 2018.)。以上都是关于碱基DNA损伤导致DNA复制突变的研究。此外,我们还研究了糖环结构改变引起的DNA损伤对DNA复制的影响。DNA复制的溶液中存在与dNTPs结构类似却浓度大大过量的rNTPs,DNA聚合酶可插入rNTPs,在DNA模板中形成rNMPs。存在rNTPs增加了DNA聚合酶的广义错配率,比传统错配率高出很多(Biochem. ***. Commun., 496:1076-1081, 2018)。意外发现,rNTPs在一定浓度下,可以促进DNA聚合酶的功能,原因是rNTPs增强了聚合酶和DNA之间的结合亲和性(JBC, 2018, Revised.)。此外,模板上的rNMPs也阻滞了T7 DNA聚合酶进行的引物延伸和T7复制体进行的链取代反应(Biochimie, 151:128-138, 2018)。

关键词： DNA复制 DNA损伤绿脓杆菌噬菌体PaP1 DNA聚合酶gp90 复制突变

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GSK3 contributes to obesity-induced adipose tissue inflammation by regulating AIM/CD5L mediated macrophage migration

GSK3 contributes to obesity-induced adipose tissue inflammat...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Li Wang Yuan Wang Chao Zhang Jingjing Li Yuan Meng Lijun Di Metabolomics Core Faculty of Health SciencesUniversity of Macau

Obesity-induced inflammation in white adipose tissue,characterized by increased macrophage infiltration and associated with macrophage population shift from anti-inflammatory M2 to proinflammatory M1 macrophages,largely contributes to obesity-induced insulin resistance and influences T2 DM ***3,a serine/threonine kinase,has been reported to participate in various cellular *** sought to examine the potential mechanism by which GSK3,a serine/threonine kinase implaicated in various cellular processes,modulates obesity-induced visceral adipose tissue(VAT) *** C57 BL/6 J mice were fed a high-fat diet for 10 weeks while being treated with control or GSK3 ***-Sequencing results using VAT demonstrated that GSK3 inhibitor treatment reversed obesity-specific expression of genes associated with ***,GSK3 inhibition reduced M1 macrophages and increased M2 macrophages in VAT,while decreasing inflammatory *** anti-inflammatory effects of GSK3 inhibition were found to be driven,at least in part,by inhibiting production of apoptosis inhibitor of macrophage(AIM) in macrophages via inactivating STAT3 to reduce free fatty acid and chemokine level produced from VAT to suppress circulatory monocyte *** findings suggest that GSK3 may act as an important regulator of obesity-induced inflammation and characterize the novel role of GSK3 in shifting macrophage polarization and reinforce its therapeutic potential for obesity-induced inflammation and its associated diabetes.

关键词： Obesity Inflammation Macrophage Insulin resistance GSK3/AIM

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SEC2 mutant drives T lymphocyte activation through PI3K/mTOR and NF-?B signaling pathways

SEC2 mutant drives T lymphocyte activation through PI3K/mTOR...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Xuanhe Fu Mingkai Xu Rong Zhang Jinghai Zhang Institute of Applied Ecology Chinese Academy of Sciences School of Life Science and Biopharmaceutics Shenyang Pharmaceutical University

Staphylococcal enterotoxin C2(SEC2) causes rapid clonal expansion of lymphocytes and secretion of T cell growth factors,leading to a severe inflammatory response within *** previous studies constructed a SEC2 mutant ST-4 with enhanced recognition of Vβ regions of T-cell receptors,which can activate increased number of T cells and produce more cytokines than ***,the signaling mechanisms of SEC2/ST-4–mediated immune activation have not been *** this study,we showed that the phosphatidylinositide-3-kinase(PI-3 K) inhibitor LY294002,mammalian target of rapamycin(mTOR) inhibitor rapamycin,and nuclear factor kappa-light-chain-enhancer of activated B cells(NF-κB) inhibitor Bay11-7085 could suppress SEC2/ST-4–induced proliferation,CD69/CD25 expression,cell-cycle progression,and IL-2 production in BALB/c mouse *** addition,we observed significantly upregulated expression of p70 S6 K,cyclin E,cyclin D3,and NF-?B/p65,but downregulated expression of p27 kip during SEC2/ST-4–driven T cells ***,SEC2/ST-4–induced changes in cell cycle and PI3 K/mTOR signaling were significantly relieved by either LY294002 or rapamycin,and the induction of NF-?B/p65 induced was significantly downregulated by ***,we found that IL-2 secretion was positively associated with p65 expression in a time-and dose-dependent *** together,our findings demonstrate the involvement of PI3 K/mTOR and NF-κB signaling pathways in SEC2/ST-4–induced T cell ***-4 intensifies PI3 K/mTOR and NF-?B signaling transduction,ultimately leading to enhance T cell *** results provide a theoretical mechanism for future immunotherapy using ST-4.

关键词： SEC2 immune response signal pathway proliferation

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DKK2 imparts tumor immunity evasion through β-catenin-independent suppression of cytotoxic immune-cell activation

DKK2 imparts tumor immunity evasion through β-catenin-indep...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Qian Xiao Jibo Wu Wei-Jia Wang Shiyang Chen Yingxia Zheng Xiaoqing Yu Katrina Meeth Mahnaz Sahraei Alfred L M Bothwell Lieping Chen Marcus Bosenberg Jianfeng Chen Veronika Sexl Le Sun Lin Li Wenwen Tang Dianqing Wu Vascular Biology and Therapeutic Program and Department of Pharmacology Yale School of Medicine State Key Laboratory of Molecular Biology CAS Center for Excellence in Molecular Cell ScienceInnovation Center for Cell Signaling NetworkInstitute of Biochemistry and Cell BiologyShanghai Institutes for Biological SciencesChinese Academy of SciencesUniversity of Chinese Academy of Sciences State Key Laboratory of Cell Biology CAS Center for Excellence in Molecular Cell ScienceShanghai Institute of Biochemistry and Cell BiologyChinese Academy of SciencesUniversity of Chinese Academy of Sciences Biostatistics Department Yale University Departments of Dermatology and Pathology Yale School of Medicine Department of Immunobiology Yale School of Medicine Yale Cancer Center Yale School of Medicine Institute of Pharmacology and Toxicology Department for Biomedical SciencesUniversity of Veterinary Medicine Vienna AbMax

Immunotherapy offers new options for cancer treatment,but efficacy varies across cancer *** cancers(CRCs) are largely refractory to immune-checkpoint blockade,which suggests the presence of yet uncharacterized immunesuppressive *** we report that the loss of adenomatosis polyposis coli(APC) in intestinal tumor cells or of the tumor suppressor PTEN in melanoma cells upregulates the expression of Dickkopf-related protein 2(DKK2),which,together with its receptor LRP5,provides an unconventional mechanism for tumor immune ***2 secreted by tumor cells acts on cytotoxic lymphocytes,inhibiting STAT5 signaling by impeding STAT5 nuclear localization via LRP5,but independently of LRP6 and the Wnt–b-catenin *** or antibody-mediated ablation of DKK2 activates natural killer(NK) cells and CD8+T cells in tumors,impedes tumor progression,and enhances the effects of PD-1 ***,we have identified a previously unknown tumor immune-suppressive mechanism and immunotherapeutic targets particularly relevant for CRCs and a subset of melanomas.

关键词： Immunotherapy DKK2 STAT5 LRP5(Times New Roman,12 points)

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Akt-induced phosphorylation of Atg4B impairs mitochondrial activity and enhances the Warburg effect in hepatocellular carcinoma cells

Akt-induced phosphorylation of Atg4B impairs mitochondrial a...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Zhenhong Ni Jintao He Yaran Wu Xufang Dai Xiaojing Yan Bo Li Xinzhe Li Haojun Xiong Jiqin Lian Fengtian He Department of Biochemistry and Molecular Biology College of Basic Medical SciencesArmy Medical University Institute of Combined Injury College of Preventive MedicineArmy Medical University College of Educational Science Chongqing Normal University

Phosphorylation is a major type of post-translational modification,which can influence the cellular physiological ***4 B,a key autophagy-related protein,has a potential effect on the survival of tumor ***,it is still unknown as to the role of Atg4 B phosphorylation in *** this study,we identified a novel phosphorylation site at Ser34 of Atg4 B induced by AKT in hepatocellular carcinoma(HCC) *** phosphorylation of Atg4 B at Ser34 had little effect on autophagic flux,but promoted the Warburg effect including the increase of L-lactate production and glucose consumption,and the decrease of oxygen consumption in HCC *** Ser34 phosphorylation of Atg4 B also contributed to the impairment of mitochondrial activity including the inhibition of F1 Fo-ATP synthase activity and the elevation of mitochondrial ROS in HCC ***,the phosphorylation of Atg4 B at Ser34 enhanced its mitochondrial location and the subsequent colocalization with F1 Fo-ATP synthase in HCC ***,recombinant human Atg4 B protein suppressed the activity of F1 Fo-ATP synthase in MgATP submitochondrial particles from patient-derived HCC tissues in *** summary,our results demonstrate for the first time that the phosphorylation of Atg4 B at Ser34 participates in the metabolic reprogramming of HCC cells via repressing mitochondrial function,which possibly results from the Ser34 phosphorylation-induced mitochondrial enrichment of Atg4 B and the subsequent inhibition of F1 Fo-ATP synthase *** findings reveal a noncanonical working pattern of Atg4 B under pathological conditions,which may provide a scientific basis for developing novel strategies for HCC treatment by targeting Atg4 B and its Ser34 phosphorylation.

关键词： Akt Atg4B Phosphorylation Warburg effect HCC

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PES1 promotes the occurrence and development of papillary thyroid cancer by upregulating the ERα/ERβ protein ratio

PES1 promotes the occurrence and development of papillary th...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议

作者： Yi-Bo Qiu Ling-Yao Liao Rong Jiang Man Xu Lin-Wan Xu George G.Chen Zhi-Min Liu Department of Biochemistry and Molecular Biology Chongqing Medical University Department of Pathology Molecular Medicine and Cancer Research CenterChongqing Medical University Department of Surgery Chinese University of Hong KongPrince of Wales Hospital

Estrogen has been suggested to play a role in the occurrence and development of papillary thyroid cancer(PTC).The balance and the ratio between ERα and ERβ protein are crucial in determining the effect of estrogen on target tissues and ***1,a BRCT domain-containing protein,has been shown to play a role in modulating the balance and the ratio between ERα and ERβ protein,which is associated with the occurrence and development of breast and ovarian ***,the role of PES1 in connection with the balance and the ratio between ERα and ERβ protein in the occurrence and development of PTC remains *** this study,PES1 protein level in human PTC tissues and cells was examined using immunohistochemistry and Western blotting,*** correlations of PES1 protein level with ERα and ERβ protein levels,with various clinicopathological features of PTC patients,with the ERα/ERβ protein ratio and the proliferation,invasion and migration of PTC cells were assessed using statistical *** results showed that ERα and ERβ were co-expressed in human PTC tissues and ***α promoted and ERβ inhibited the proliferation,invasion and migration of PTC cells and a Yin-Yang balance existed between ERα and ERβ.PES1 modulated this Yin-Yang balance by elevating ERα and reducing ERβ protein level,then upregulating the ERα/ERβ protein ratio and promoting the proliferation,invasion and migration of PTC *** PTC tissues,PES1 protein level positively correlated with ERα(rs = 0.549,P < 0.001) and negatively correlated with ERβ protein level(rs =-0.353,P < 0.001).PES1 and ERα protein levels were gradually increased and ERβ protein level was decreased by degree in the occurrence and development of *** PES1 and ERα and decreased ERβ protein levels correlated with aggressive PTC behaviors such as large tumor size,extrathyroidal extension(ETE),lymph node metastasis(LNM) and high TNM *** was suggested that PES1 promotes the occurrence and development of P

关键词： PES1 ERα ERβ papillary thyroid cancer

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