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Potential of electron transfer and its application in dictating routes of biochemical processes associated with metabolic reprogramming

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Frontiers of Medicine 2021年第5期15卷 679-692页

作者： Ronghui Yang guoguang ying Binghui Li Department of Biochemistry and Molecular Biology Capital Medical UniversityBeijing 100069China Advanced Innovation Center for Human Brain Protection Capital Medical UniversityBeijing 100069China Beijing Key Laboratory for Tumor Invasion and Metastasis Capital Medical UniversityBeijing 100069China Department of Cancer Cell Biology Tianjin Medical University Cancer Institute and HospitalTianjin 300060China Key Laboratory of Breast Cancer Prevention and Therapy Tianjin Medical UniversityMinistry of EducationTianjin 300060China National Clinical Research Center for Cancer Tianjin Medical University Cancer Institute and HospitalTianjin 300060China

Metabolic reprogramming,such as abnormal utilization of glucose,addiction to glutamine,and increased de-novo lipid synthesis,extensively occurs in proliferating cancer cells,but the underneath rationale has remained to be *** on the concept of the degree of reduction of a compound,we have recently proposed a calculation termed as potential of electron transfer(PET),which is used to characterize the degree of electron redistribution coupled with metabolic *** this calculation is combined with the assumed model of electron balance in a cellular context,the enforced selective reprogramming could be predicted by examining the net changes of the PET values associated with the biochemical pathways in anaerobic *** interesting properties of PET in cancer cells were also discussed,and the model was extended to uncover the chemical nature underlying aerobic glycolysis that essentially results from energy requirement and electron *** electron transfer could drive metabolic reprogramming in cancer ***,the concept and model established on electron transfer could guide the treatment strategies of tumors and future studies on cellular metabolism.

关键词： metabolic reprogramming potential of electron transfer cell proliferation aerobic glycolysis cancer metabolism

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Exosomal miR-155 from gastric cancer induces cancerassociated cachexia by suppressing adipogenesis and promoting brown adipose differentiation via C/EPBβ

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Cancer Biology & Medicine 2022年第9期19卷 1301-1314页

作者： ying Liu Meng Wang Ting Deng Rui Liu Tao Ning Ming Bai guoguang ying Haiyang Zhang Yi Ba Tianjin Medical University Cancer Institute and Hospital National Clinical Research Center for CancerTianjin’s Clinical Research Center for CancerKey Laboratory of Cancer Prevention and TherapyTianjin 300060China

Objective:The aim of this research was to identify whether exosomes were involved in impairing adipogenesis in cancer-associated cachexia(CAC)by detecting the adipodifferentiation capacity and the expressions of adipogenic proteins in gastric cancer(GC)-associated ***:Western blotting and RT-PCR were used to investigate the expressions of C/EPBβ,C/EPBα,PPARγ,and UCP1 in adipose mesenchymal stem cells(A-MSCs)to evaluate the function of exosomal ***/c nude mice were intravenously injected in vivo with GC exosomes with different levels of miR-155 to determine changes in adipodifferentiation of ***:Exosomes derived from GC cells suppressed adipogenesis in A-MSCs as characterized by decreased lipid ***,A-MSCs co-cultured with GC exosomes exhibited increased ATP production through brown adipose differentiation characterized by highly dense mitochondria and enhanced UCP1 expression(P<0.05).Mechanistically,exosomal miR-155 secreted from GC cells suppressed adipogenesis and promoted brown adipose differentiation by targeting C/EPBβ,accompanied by downregulated C/EPBαand PPARγand upregulated UCP1(P<0.05).Moreover,overexpression of miR-155 in GC exosomes improved CAC in vivo,which was characterized by fat loss,suppressed expressions of C/EPBβ,C/EPBα,and PPARγin A-MSCs,and high expression of UCP1(P<0.05).Decreasing the level of miR-155 in injected GC exosomes abrogated the improved CAC ***:GC exosomal miR-155 suppressed adipogenesis and enhanced brown adipose differentiation in A-MSCs by targeting C/EPBβof A-MSCs,which played a crucial role in CAC.

关键词： Exosomes adipose mesenchymal stem cells miR-155 cachexia gastric cancer

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Determination of glucose deficiency-induced cell death by mitochondrial ATP generation-driven proton homeostasis

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Journal of Molecular Cell Biology 2017年第5期9卷 395-408页

作者： Yanfen Cui Yuanyuan Wang Miao Liu Li Qiu Pan Xing Xin Wang guoguang ying Binghui Li Laboratory of Cancer Cell Biology Key Laboratory of Breast Cancer Prevention and Therapy National Clinical Research Center for Cancer Tianjin MedicalUniversity Cancer Institute and Hospital Tianjin 300060 China The First Department of Breast Tumor Key Laboratory of Breast Cancer Prevention and Therapy National Clinical Research Center for Cancer Tianjin MedicalUniversity Cancer Institute and Hospital Tianjin 300060 China

Glucose is one of major nutrients and its catabolism provides energy and/or building bricks for cell proliferation. Glucose deficiency results in cell death. However, the underlying mechanism still remains elusive. By using our recently developed method to monitor real-time cellular apoptosis and necrosis, we show that glucose deprivation can directly elicit necrosis, which is promoted by mito- chondrial impairment, depending on mitochondrial adenosine triphosphate （ATP） generation instead of ATP depletion. We demon- strate that glucose metabolism is the major source to produce protons. Glucose deficiency leads to lack of proton provision while mitochondda[ electron transfer chain continues consuming protons to generate energy, which provokes a compensatory lysosomal proton efflux and resultant increased lysosomal pH. This [ysosomal aikaUnization can trigger apoptosis or necrosis depending on the extent of alkalinization. Taken together, our results build up a metabolic connection between glycolysis, mitochondrion, and iysosome, and reveal an essential role of glucose metabolism in maintaining proton homeostasis to support cell survival.

关键词： glucose deficiency apoptosis necrosis proton homeostasis

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PKM2 promotes reductive glutamine metabolism

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Cancer Biology & Medicine 2018年第4期15卷 389-399页

作者： Miao Liu Yuanyuan Wang Yuxia Ruan Changsen Bai Li Qiu Yanfen Cui guoguang ying Binghui Li Department of Cancer Cell Biology Tianjin Medical University Cancer Institute and HospitalNational Clinical Research Center for CancerKey Laboratory of Cancer Prevention and TherapyTianjinTianjin’s Clinical Research Center for CancerTianjin 300060China Department of Biochemistry and Molecular Biology Capital Medical UniversityBeijing 100069China

Objective:Pyruvate kinases M(PKM),including the PKM1 and PKM2 isoforms,are critical factors in glucose ***2promotes aerobic glycolysis,a phenomenon known as"the Warburg effect".The purpose of this study was to identify the roles of PKM2 in regulating cellular ***:The CRISPR/Cas9 system was used to generate the PKM-knockout cell model to evaluate the role of PKM in cellular *** levels were measured by the Vitros LAC slide method on an autoanalyzer and glucose levels were measured by the autoanalyzer *** metabolism of ^(13)C_6-glucose or ^(13)C_5-glutamine was evaluated by liquid chromatography/mass spectrometry *** effects of PKM on tumor growth were detected in vivo in a tumor-bearing mouse ***:We found that both PKM1 and PKM2 enabled aerobic glycolysis,but PKM2 converted glucose to lactate much more efficiently than *** a result,PKM2 reduced glucose levels reserved for intracellular utilization,particularly for the production of citrate,and thus increased theα-ketoglutarate/citrate ratio to promote the generation of glutamine-derived acetylcoenzyme A through the reductive ***,reductive glutamine metabolism facilitated cell proliferation under hypoxia conditions,which supports in vivo tumor *** addition,PKM-deletion induced a reverse Warburg effect in tumorassociated stromal ***:PKM2 plays a critical role in promoting reductive glutamine metabolism and maintaining proton *** study is helpful to increase the understanding of the physiological role of PKM2 in cancer cells.

关键词： The Warburg effect the reverse Warburg effect PKM2 glucose metabolism proton homeostasis

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Onco-miR-24 regulates cell growth and apoptosis by targeting BCL2L11 in gastric cancer

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Protein & Cell 2016年第2期7卷 141-151页

作者： Haiyang Zhang Jingjing Duan Yanjun Qu Ting Deng Rui Liu Le Zhang Ming Bai Jialu Li Tao Ning Shaohua Ge Xia Wang ZhenzhenWang~ Qian Fan Hongli Li guoguang ying Dingzhi Huang Yi Ba Tianjin Medical University Cancer Institute and Hospital Key Laboratory of Cancer Prevention and Therapy National ClinicalResearch Center for Cancer Tianjin 300060 China Department of Gastroenterology Tianjin First Center Hospital Tianjin 300192 China Changchun GeneScience Pharmaceuticals Co. Ltd Changchun 130012 China

Gastric cancer is one of the most common malignancies worldwide; however, the molecular mechanism in tumorigenesis still needs exploration. BCL2L11 belongs to the BCL-2 family, and acts as a central regulator of the intrinsic apoptotic cascade and mediates cell apoptosis. Although miRNAs have been reported to be involved in each stage of cancer development, the role of miR-24 in GC has not been reported yet. In the present study, miR- 24 was found to be up-regulated while the expression of BCL2L11 was inhibited in tumor tissues of GC. Studies from both in vitro and in vivo shown that miR-24 regulates BCL2L11 expression by directly binding with 3＇UTR of mRNA, thus promoting cell growth, migration while inhibiting cell apoptosis. Therefore, miR-24 is a novel onco-miRNA that can be potential drug targets for future clinical use.

关键词： gastric cancer BCL2L11 miR-24,tumorigenesis cell apoptosis proliferation migration

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“教学管理软件包”系统的设计及应用

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四川工业学院学报 1993年第4期12卷 289-297页

作者：崔国光邹英四川工业学院电精机教研室四川工业学院教务处电教室

本文讨论了“教学管理软件包”程序的设计要求、特点、主要功能及其应用,以及根据教学管理的需要,如何对软件进行特殊处理的方法。该软件包已在我院成功地应用多年,并在四川省数所高校推广应用,得到了用户的好评,是一套实用的教学管理... 详细信息

本文讨论了“教学管理软件包”程序的设计要求、特点、主要功能及其应用,以及根据教学管理的需要,如何对软件进行特殊处理的方法。该软件包已在我院成功地应用多年,并在四川省数所高校推广应用,得到了用户的好评,是一套实用的教学管理软件。

关键词：数据库教学管理软件包

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EHD2干扰影响永生化乳腺上皮细胞的增殖和迁移

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中国肿瘤临床 2011年第11期38卷 601-604页

作者：王洪玉郭立莎吴敏徐玥董秋萍应国光天津医科大学附属肿瘤医院肿瘤研究所中心实验室乳腺癌防治教育部重点实验室天津市肿瘤防治重点实验室天津市300060

目的:研究EHD2膜转运调控蛋白对非癌乳腺上皮细胞HBL100生长、粘附和迁移等生物学行为的影响,揭示乳腺癌发生发展的新分子机制。方法:数据挖掘分析已公开的各组乳腺癌基因表达芯片结果中EHD2基因表达与乳腺肿瘤发生发展的关系。小RNA干... 详细信息

目的:研究EHD2膜转运调控蛋白对非癌乳腺上皮细胞HBL100生长、粘附和迁移等生物学行为的影响,揭示乳腺癌发生发展的新分子机制。方法:数据挖掘分析已公开的各组乳腺癌基因表达芯片结果中EHD2基因表达与乳腺肿瘤发生发展的关系。小RNA干扰永生化非癌乳腺上皮细胞HBL100的EHD2蛋白表达水平,免疫印迹法检测验证EHD2蛋白的降表达情况,并以此为模型研究EHD2干扰表达对细胞的增殖速度、粘附能力以及迁移能力等生物学行为的影响。结果:数据挖掘结果显示,EHD2基因在乳腺癌中的表达明显减弱,而且其表达水平随肿瘤病理分级的升高呈逐级下降趋势。HBL100细胞系小RNA干扰EHD2表达后,二维培养条件下的生长及EGF诱导下的迁移速度均升高,差异有统计学意义(P<0.005),但其粘附能力下降(P<0.05)。结论:EHD2参与调节永生化乳腺上皮细胞HBL100的生长、粘附和迁移。在乳腺肿瘤中EHD2的基因表达失调下降,提示EHD2可能是一个新的乳腺抑癌基因,并可能成为乳腺癌分子诊断和靶向治疗的新指标、新靶点。

关键词： EHD2 增殖粘附迁移乳腺癌

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顺铂诱导耐药蛋白BCRP与EHD2表达上调并在细胞表面的富集

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中国肿瘤临床 2013年第21期40卷 1284-1287页

作者：李盼潘利付欣杨少斌冯婧文胡明秋应国光天津医科大学肿瘤医院肿瘤研究所肿瘤细胞生物学实验室国家肿瘤临床医学研究中心天津市肿瘤防治重点实验室天津市300060 海洋石油总医院

目的:建立顺铂耐受的人肺腺癌A549/DDP细胞株,研究EHD2(EH domain-containing protein-2)与肿瘤细胞药物耐受的潜在关系。方法:以DDP为诱导剂,采用低浓度逐步增量诱导方法建立人肺癌耐药细胞系A549/DDP,采用MTT法测定药物敏感性,免疫印... 详细信息

目的:建立顺铂耐受的人肺腺癌A549/DDP细胞株,研究EHD2(EH domain-containing protein-2)与肿瘤细胞药物耐受的潜在关系。方法:以DDP为诱导剂,采用低浓度逐步增量诱导方法建立人肺癌耐药细胞系A549/DDP,采用MTT法测定药物敏感性,免疫印迹法检测耐药蛋白BCRP及EHD2蛋白的表达水平,免疫荧光方法检测BCRP及EHD2的细胞定位。结果:成功建立DDP耐药细胞系A549/DDP,对DDP的耐药指数为7.6;免疫印迹结果显示BCRP在耐药细胞系A549/DDP中的表达明显高于其亲本细胞A549,EHD2蛋白在耐药细胞系的表达略有增高;免疫荧光成像显示EHD2蛋白在细胞膜表面富集,并与BCRP耐药蛋白共定位。结论:BCRP和EHD2在获得性耐药细胞中富集,并于细胞膜表面共定位,提示内吞蛋白EHD2可能调控耐药蛋白BCRP的膜稳定性,从而介导肿瘤细胞耐药。

关键词： BCRP EHD2 肿瘤耐药

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EHD2调节乳腺上皮细胞极性的实验研究

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中国肿瘤临床 2011年第11期38卷 608-611页

作者：郭立莎王洪玉吴敏徐玥董秋萍应国光天津医科大学附属肿瘤医院肿瘤研究所中心实验室乳腺癌防治教育部重点实验室天津市肿瘤防治重点实验室天津市300060

目的:研究EHD2基因对上皮细胞极性的调控作用及其机制,探讨EHD2基因在乳腺癌组织中表达失调的肿瘤分子生物学和细胞生物学意义。方法:以乳腺永生化正常上皮细胞的二维和三维培养为模型,建立EHD2突变体的Doxycycline外源诱导表达体系,应... 详细信息

目的:研究EHD2基因对上皮细胞极性的调控作用及其机制,探讨EHD2基因在乳腺癌组织中表达失调的肿瘤分子生物学和细胞生物学意义。方法:以乳腺永生化正常上皮细胞的二维和三维培养为模型,建立EHD2突变体的Doxycycline外源诱导表达体系,应用荧光显微镜和激光共聚焦显微成像技术,观察诱导表达前后细胞在二维培养条件下细胞内β肌动蛋白的微丝组装及聚合情况,以及三维基质胶培养条件下对上皮细胞腺泡形成的影响,综合判断EHD2蛋白在调控上皮细胞极性中的生物学作用。结果:EHD2突变的诱导表达显著影响乳腺上皮细胞的骨架重排,在细胞表面发生密集发散状微刺,细胞内定向排列的β肌动蛋白微丝结构消失。三维培养中,EHD2突变体的引入破坏了原本规则的腺泡型生长,细胞向外侵入基质。结论:EHD2突变可导致乳腺上皮细胞的骨架重排和极性改变,可能是乳腺肿瘤发生的重要机制之一。

关键词： EHD2 乳腺上皮细胞极性

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From complexity to clarity: development of CHM-FIEFP for predicting effective components in Chinese herbal formulas by using big data

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Cancer Biology & Medicine 2024年第11期 1067-1077页

作者： Boyu Pan Han Zhu Jiaqi Yang Liangjiao Wang Zizhen Chen Jian Ma Bo Zhang Zhanyu Pan guoguang ying Shao Li Liren Liu Department of Molecular Pharmacology Tianjin Medical University Cancer Institute & Hospital National Clinical Research Center for Cancer Key Laboratory of Cancer Prevention and TherapyTianjin Tianjin's Clinical Research Center for Cancer College of Electronic and Information Engineering Shanghai Research Institute for Intelligent Autonomous Systems Tongji University Department of General Surgery Tianjin Haihe Hospital Beijing Intelligent Medicine and Network Pharmacology Co. Ltd Institute for TCM-X MOE Key Laboratory of Bioinformatics Bioinformatics Division BNRist Department of AutomationTsinghua University Department of Integrative Oncology Tianjin Medical University Cancer Institute and Hospital Laboratory of Cancer Cell Biology Tianjin Medical University Cancer Institute & Hospital

Objective: The presence of complex components in Chinese herbal medicine(CHM) hinders identification of the primary active substances and understanding of pharmacological principles. This study was aimed at developing a big-data-based, knowledgedriven in silico algorithm for predicting central components in complex CHM ***: Network pharmacology(TCMSP) and clinical(GEO) databases were searched to retrieve gene targets corresponding to the formula ingredients, herbal components, and specific disease being treated. Intersections were determined to obtain diseasespecific core targets, which underwent further GO and KEGG enrichment analyses to generate non-redundant biological processes and molecular targets for the formula and each component. The ratios of the numbers of biological and molecular events associated with a component were calculated with a formula, and entropy weighting was performed to obtain a fitting score to facilitate ranking and improve identification of the key components. The established method was tested on the traditional CHM formula Danggui Sini Decoction(DSD) for gastric cancer. Finally, the effects of the predicted critical component were experimentally validated in gastric cancer ***: An algorithm called Chinese Herb Medicine-Formula vs. Ingredients Efficacy Fitting & Prediction(CHM-FIEFP) was developed. Ferulic acid was identified as having the highest fitting score among all tested DSD components. The pharmacological effects of ferulic acid alone were similar to those of ***: CHM-FIEFP is a promising in silico method for identifying pharmacological components of CHM formulas with activity against specific diseases. This approach may also be practical for solving other similarly complex problems. The algorithm is available at http://***/.

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