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| 1 | Oxidative stress and diabetes:antioxidative strategies显示文摘Diabetes mellitus is one of the major public health problems worldwide.Considerable recent evidence suggests that the cellular reduction-oxidation(redox)imbalance leads to oxidative stress and subsequent occurrence and development of diabetes and related complications by regulating certain signaling pathways involved in p-cell dysfunction and insulin resistance.Reactive oxide species(ROS)can also directly oxidize certain proteins(defined as redox modification)involved in the diabetes process.There are a number of potential problems in the clinical application of antioxidant therapies including poor solubility,storage instability and nonselectivity of antioxidants.Novel antioxidant delivery systems may overcome pharmacokinetic and stability problem and improve the selectivity of scavenging ROS.We have therefore focused on the role of oxidative stress and antioxidative therapies in the pathogenesis of diabetes mellitus.Precise therapeutic interventions against ROS and downstream targets are now possible and provide important new insights into the treatment of diabetes. | Pengju Zhang Tao Li Xingyun Wu Edouard C.Nice Canhua Huang Yuanyuan Zhang | 2020 | Frontiers of Medicine2020，14，5： | 29 |
| 2 | Spontaneous apoptosis of cells in therapeutic stem cell preparation exert immunomodulatory effects through release of phosphatidylserine显示文摘Mesenchymal stem cell(MSC)-mediated immunomodulation has been harnessed for the treatment of human diseases,but its underlying mechanism has not been fully understood.Dead cells,including apoptotic cells have immunomodulatory properties.It has been repeatedly reported that the proportion of nonviable MSCs in a MSC therapeutic preparation varied from 5-50%in the ongoing clinical trials.It is conceivable that the nonviable cells in a MSC therapeutic preparation may play a role in the therapeutic effects of MSCs.We found that the MSC therapeutic preparation in the present study had about 5%dead MSCs(DMSCs),characterized by apoptotic cells.Namely,1×10^(6) MSCs in the preparation contained about 5×10^(4) DMSCs.We found that the treatment with even 5×10^(4) DMSCs alone had the equal therapeutic effects as with 1×10^(6) MSCs.This protective effect of the dead MSCs alone was confirmed in four mouse models,including concanavalin A(ConA)-and carbon tetrachloride(CCI4)-induced acute liver injury,LPS-induced lung injury and spinal cord injury.We also found that the infused MSCs died by apoptosis in vivo.Furthermore,the therapeutic effect was attributed to the elevated level of phosphatidylserine(PS)upon the injection of MSCs or DMSCs.The direct administration of PS liposomes(PSLs)mimic apoptotic cell fragments also exerted the protective effects as MSCs and DMSCs.The Mer tyrosine kinase(MerTK)deficiency or the knockout of chemokine receptor C-C motif chemokine receptor 2(CCR2)reversed these protective effects of MSCs or DMSCs.These results revealed that DMSCs alone in the therapeutic stem cell preparation or the apoptotic cells induced in vivo may exert the same immunomodulatory property as the'living MSCs preparation'through releasing PS,which was further recognized by MerTK and participated in modulating immune cells. | Xuemei He Weiqi Hong Jingyun Yang Hong Lei Tianqi Lu Cai He Zhenfei Bi Xiangyu Pan Yu Liu Lunzhi Dai Wei Wang Canhua Huang Hongxin Deng Xiawei Wei | 2021 | Signal Transduction and Targeted Therapy2021，6，8： | 6 |
| 3 | NAD+metabolism:pathophysiologic mechanisms and therapeutic potential显示文摘Nicotinamide adenine dinucleotide(NAD^(+))and its metabolites function as critical regulators to maintain physiologic processes,enabling the plastic cells to adapt to environmental changes including nutrient perturbation,genotoxic factors,circadian disorder,infection,inflammation and xenobiotics.These effects are mainly achieved by the driving effect of NAD^(+)on metabolic pathways as enzyme cofactors transferring hydrogen in oxidation-reduction reactions.Besides,multiple NAD^(+)-dependent enzymes are involved in physiology either by post-synthesis chemical modification of DNA,RNA and proteins,or releasing second messenger cyclic ADPribose(cADPR)and NAADP^(+).Prolonged disequilibrium of NAD^(+)metabolism disturbs the physiological functions,resulting in diseases including metabolic diseases,cancer,aging and neurodegeneration disorder.In this review,we summarize recent advances in our understanding of the molecular mechanisms of NAD^(+)-regulated physiological responses to stresses,the contribution of NAD^(+)deficiency to various diseases via manipulating cellular communication networks and the potential new avenues for therapeutic intervention. | Na Xie Lu Zhang Wei Gao Canhua Huang Peter Ernst Huber Xiaobo Zhou Changlong Li Guobo Shen Bingwen Zou | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 5 |
| 4 | Redox regulation in tumor cell epithelial-mesenchymal transition:molecular basis and therapeutic strategy显示文摘Epithelial–mesenchymal transition(EMT)is recognized as a driving force of cancer cell metastasis and drug resistance,two leading causes of cancer recurrence and cancer-related death.It is,therefore,logical in cancer therapy to target the EMT switch to prevent such cancer metastasis and recurrence.Previous reports have indicated that growth factors(such as epidermal growth factor and fibroblast growth factor)and cytokines(such as the transforming growth factor beta(TGF-β)family)are major stimulators of EMT.However,the mechanisms underlying EMT initiation and progression remain unclear.Recently,emerging evidence has suggested that reactive oxygen species(ROS),important cellular secondary messengers involved in diverse biological events in cancer cells,play essential roles in the EMT process in cancer cells by regulating extracellular matrix(ECM)remodeling,cytoskeleton remodeling,cell–cell junctions,and cell mobility.Thus,targeting EMT by manipulating the intracellular redox status may hold promise for cancer therapy.Herein,we will address recent advances in redox biology involved in the EMT process in cancer cells,which will contribute to the development of novel therapeutic strategies by targeting redox-regulated EMT for cancer treatment. | Jingwen Jiang Kui Wang Yan Chen Haining Chen Edouard C Nice Canhua Huang | 2017 | Signal Transduction and Targeted Therapy2017，2，1： | 5 |
| 5 | Cancer metabolism and tumor microenvironment:fostering each other?显示文摘The changes associated with malignancy are not only in cancer cells but also in environment in which cancer cells live.Metabolic reprogramming supports tumor cells’high demand of biogenesis for their rapid proliferation,and helps tumor cells to survive under certain genetic or environmental stresses.Emerging evidence suggests that metabolic alteration is ultimately and tightly associated with genetic changes,in particular the dysregulation of key oncogenic and tumor suppressive signaling pathways.Cancer cells activate HIF signaling even in the presence of oxygen and in the absence of growth factor stimulation.This cancer metabolic phenotype,described firstly by German physiologist Otto Warburg,ensures enhanced glycolytic metabolism for the biosynthesis of macromolecules.The conception of metabolite signaling,i.e.,metabolites are regulators of cell signaling,provides novel insights into how reactive oxygen species(ROS)and other metabolites deregulation may regulate redox homeostasis,epigenetics,and proliferation of cancer cells.Moreover,the unveiling of noncanonical functions of metabolic enzymes,such as the moonlighting functions of phosphoglycerate kinase 1(PGK1),reassures the importance of metabolism in cancer development.The metabolic,microRNAs,and ncRNAs alterations in cancer cells can be sorted and delivered either to intercellular matrix or to cancer adjacent cells to shape cancer microenvironment via media such as exosome.Among them,cancer microenvironmental cells are immune cells which exert profound effects on cancer cells.Understanding of all these processes is a prerequisite for the development of a more effective strategy to contain cancers. | Yiyuan Yuan Huimin Li Wang Pu Leilei Chen Dong Guo Hongfei Jiang Bo He Siyuan Qin Kui Wang Na Li Jingwei Feng Jing Wen Shipeng Cheng Yaguang Zhang Weiwei Yang Dan Ye Zhimin Lu Canhua Huang Jun Mei Hua-Feng Zhang Ping Gao Peng Jiang Shicheng Su Bing Sun Shi-Min Zhao | 2022 | Science China(Life Sciences)2022，65，2： | 5 |
| 6 | The pathogenesis and diagnosis of sepsis post burn injury显示文摘Burn is an under-appreciated trauma that is associated with unacceptably high morbidity and mortality.Although the survival rate after devastating burn injuries has continued to increase in previous decades due to medical advances in burn wound care,nutritional and fluid resuscitation and improved infection control practices,there are still large numbers of patients at a high risk of death.One of the most common complications of burn is sepsis,which is defined as“severe organ dysfunction attributed to host’s disordered response to infection”and is the primary cause of death in burn patients.Indeed,burn injuries are accompanied by a series of events that lead to sepsis and multiple organ dysfunction syndrome,such as a hypovolaemic state,immune and inflammatory responses and metabolic changes.Therefore,clear diagnostic criteria and predictive biomarkers are especially important in the prevention and treatment of sepsis and septic shock.In this review,we focus on the pathogenesis of burn wound infection and the post-burn events leading to sepsis.Moreover,the clinical and promising biomarkers of burn sepsis will also be summarized. | Pengju Zhang Bingwen Zou Yih-Cherng Liou Canhua Huang | 2021 | Burns & Trauma2021，9，1： | 5 |
| 7 | Managing the immune microenvironment of osteosarcoma:the outlook for osteosarcoma treatment显示文摘Osteosarcoma,with poor survival after metastasis,is considered the most common primary bone cancer in adolescents.Notwithstanding the efforts of researchers,its five-year survival rate has only shown limited improvement,suggesting that existing therapeutic strategies are insufficient to meet clinical needs.Notably,immunotherapy has shown certain advantages over traditional tumor treatments in inhibiting metastasis.Therefore,managing the immune microenvironment in osteosarcoma can provide novel and valuable insight into the multifaceted mechanisms underlying the heterogeneity and progression of the disease.Additionally,given the advances in nanomedicine,there exist many advanced nanoplatforms for enhanced osteosarcoma immunotherapy with satisfactory physiochemical characteristics.Here,we review the classification,characteristics,and functions of the key components of the immune microenvironment in osteosarcoma.This review also emphasizes the application,progress,and prospects of osteosarcoma immunotherapy and discusses several nanomedicine-based options to enhance the efficiency of osteosarcoma treatment.Furthermore,we examine the disadvantages of standard treatments and present future perspectives for osteosarcoma immunotherapy. | Hailong Tian Jiangjun Cao Bowen Li Edouard CNice Haijiao Mao Yi Zhang Canhua Huang | 2023 | Bone Research2023，11，1： | 3 |
| 8 | Various atomic structures of monolayer silicene fabricated on Ag(111)显示文摘 | Zhi-Long Liu Mei-Xiao Wang Jin-Peng Xu Jian-Feng Ge Guy Le Lay Patrick Vogt Dong Qian Chun-Lei Gao Canhua Liu Jin-Feng Jia | 2014 | New Journal of Physics2014，，： | 3 |
| 9 | Viral proteomics: The emerging cutting-edge of virus research显示文摘Viruses replicate and proliferate in host cells while continuously adjusting to and modulating the host environment.They encode a wide spectrum of multifunctional proteins,which interplay with and modify proteins in host cells.Viral genomes were chronologically the first to be sequenced.However,the corresponding viral proteomes,the alterations of host proteomes upon viral infection,and the dynamic nature of proteins,such as post-translational modifications,enzymatic cleavage,and activation or destruction by proteolysis,remain largely unknown.Emerging high-throughput techniques,in particular quantitative or semi-quantitative mass spectrometry-based proteomics analysis of viral and cellular proteomes,have been applied to define viruses and their interactions with their hosts.Here,we review the major areas of viral proteomics,including virion proteomics,structural proteomics,viral protein interactomics,and changes to the host cell proteome upon viral infection. | ZHOU ShengTao LIU Rui ZHAO Xia HUANG CanHua WEI YuQuan | 2011 | Science China(Life Sciences)2011，54，6： | 3 |
| 10 | Cross-cumulant enhanced radiality nanoscopy for multicolor superresolution subcellular imaging显示文摘Fluorescence fuctuation-based superresolution techniques can achieve fast superresolution imaging on a cost-effective wide-field platform at a low light level with reduced phototoxicity.However,the current methods exhibit certain imaging deficiencies that misinterpret nanoscale features reconstructed from fluctuating image scquences,thus degrading the superresolution imaging quality and performance.Here we propose Cross-cumulant enhanced radiality nanoscopy(CERN),which employs cross cumulant analysis in tandem with radiality processing.We demonstrated that CERN can significantly improve the spatial resolution at a low light level while eliminating the misinterpretations of nanoscale features of the existing fluctuation-based superresolution methods.In the experiment,we further verified the superior performance of CERN over the current methods through performing multicolor superresolution imaging of subcellular microtubule networks and clathrin-coated pits as well as the high-precision reconstruction of densely packed RNA transcripts. | ZHIPING ZENG JING MA CANHUA Xu | 2020 | Photonics Research2020，8，6： | 2 |
| 11 | BCL7C suppresses ovarian cancer growth by inactivating mutant p53显示文摘B-cell CLL/lymphoma 7 protein family member C (BCL7C) located at chromosome 16p11.2 shares partial sequence homology with the other two family members, BCL7A and BCL7B. Its role in cancer remains completely unknown. Here, we report our finding of its tumor-suppressive role in ovarian cancer. Supporting this is that BCL7C is downregulated in human ovarian carcinomas, and its underexpression is associated with unfavorable prognosis of ovarian cancer as well as some other types of human cancers. Also, ectopic BCL7C restrains cell proliferation and invasion of ovarian cancer cells. Consistently, depletion of BCL7C reduces apoptosis and promotes cell proliferation and invasion of these cancer cells. Mechanistically, BCL7C suppresses mutant p53-mediated gene transcription by binding to mutant p53, while knockdown of BCL7C enhances the expression of mutant p53 target genes in ovarian cancer cells. Primary ovarian carcinomas that sustain low levels of BCL7C often show the elevated expression of mutant p53 target genes. In line with these results, BCL7C abrogates mutant p53-induced cell proliferation and invasion, but had no impact on proliferation and invasion of cancer cells with depleted p53 or harboring wild-type p53. Altogether, our results demonstrate that BCL7C can act as a tumor suppressor to prevent ovarian tumorigenesis and progression by counteracting mutant p53 activity. | Canhua Huang Qian Hao Getao Shi Xiang Zhou Yu Zhang | 2021 | Journal of Molecular Cell Biology2021，13，2： | 2 |
| 12 | Emerging role of tumor cell plasticity in modifying therapeutic response显示文摘Resistance to cancer therapy is a major barrier to cancer management.Conventional views have proposed that acquisition of resistance may result from genetic mutations.However,accumulating evidence implicates a key role of non-mutational resistance mechanisms underlying drug tolerance,the latter of which is the focus that will be discussed here.Such non-mutational processes are largely driven by tumor cell plasticity,which renders tumor cells insusceptible to the drug-targeted pathway,thereby facilitating the tumor cell survival and growth.The concept of tumor cell plasticity highlights the significance of re-activation of developmental programs that are closely correlated with epithelial–mesenchymal transition,acquisition properties of cancer stem cells,and transdifferentiation potential during drug exposure.From observations in various cancers,this concept provides an opportunity for investigating the nature of anticancer drug resistance.Over the years,our understanding of the emerging role of phenotype switching in modifying therapeutic response has considerably increased.This expanded knowledge of tumor cell plasticity contributes to developing novel therapeutic strategies or combination therapy regimens using available anticancer drugs,which are likely to improve patient outcomes in clinical practice. | Siyuan Qin Jingwen Jiang Yi Lu Edouard CNice Canhua Huang Jian Zhang Weifeng He | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 2 |
| 13 | Histones released by NETosis enhance the infectivity of SARS-CoV-2 by bridging the spike protein subunit 2 and sialic acid on host cells显示文摘Neutrophil extracellular traps(NETs)can capture and kill viruses,such as influenza viruses,human immunodeficiency virus(HIV),and respiratory syncytial virus(RSV),thus contributing to host defense.Contrary to our expectation,we show here that the histones released by NETosis enhance the infectivity of SARS-CoV-2,as found by using live SARS-CoV-2 and two pseudovirus systems as well as a mouse model.The histone H3 or H4 selectively binds to subunit 2 of the spike(S)protein,as shown by a biochemical binding assay,surface plasmon resonance and binding energy calculation as well as the construction of a mutant S protein by replacing four acidic amino acids.Sialic acid on the host cell surface is the key molecule to which histones bridge subunit 2 of the S protein.Moreover,histones enhance cell-cell fusion.Finally,treatment with an inhibitor of NETosis,histone H3 or H4,or sialic acid notably affected the levels of sgRNA copies and the number of apoptotic cells in a mouse model.These findings suggest that SARS-CoV-2 could hijack histones from neutrophil NETosis to promote its host cell attachment and entry process and may be important in exploring pathogenesis and possible strategies to develop new effective therapies for COVID-19. | Weiqi Hong Jingyun Yang Jun Zou Zhenfei Bi Cai He Hong Lei Xuemei He Xue Li Aqu Alu Wenyan Ren Zeng Wang Xiaohua Jiang Kunhong Zhong Guowen Jia Yun Yang Wenhai Yu Qing Huang Mengli Yang Yanan Zhou Yuan Zhao Dexuan Kuang Junbin Wang Haixuan Wang Siyuan Chen Min Luo Ziqi Zhang Tiangi Lu Li Chen Haiying Que Zhiyao He Qiu Sun Wei Wang Guobo Shen Guangwen Lu Zhiwei Zhao Li Yang Jinliang Yang Zhenling Wang Jiong Li Xiangrong Song Lunzhi Dai Chong Chen Jia Geng Maling Gou Lu Chen Haohao Dong Yong Peng Canhua Huang Zhiyong Qian Wei Cheng Changfa Fan Yuquan Wei Zhaoming Su Aiping Tong Shuaiyao Lu Xiaozhong Peng Xiawei Wei | 2022 | Cellular & Molecular Immunology2022，19，5： | 2 |
| 14 | Repurposing econazole as a pharmacological autophagy inhibitor to treat pancreatic ductal adenocarcinoma显示文摘Pancreatic ductal adenocarcinoma(PDAC)is characterized by the highest mortality among carcinomas.The pathogenesis of PDAC requires elevated autophagy,inhibition of which using hydroxychloroquine has shown promise.However,current realization is impeded by its suboptimal use and unpredictable toxicity.Attempts to identify novel autophagy-modulating agents from already approved drugs offer a rapid and accessible approach.Here,using a patient-derived organoid model,we performed a comparative analysis of therapeutic responses among various antimalarial/fungal/parasitic/viral agents,through which econazole(ECON),an antifungal compound,emerged as the top candidate.Further testing in cell-line and xenograft models of PDAC validated this activity,which occurred as a direct consequence of dysfunctional autophagy.More specifically,ECON boosted autophagy initiation but blocked lysosome biogenesis.RNA sequencing analysis revealed that this autophagic induction was largely attributed to the altered expression of activation transcription factor 3(ATF3).Increased nuclear import of ATF3 and its transcriptional repression of inhibitor of differentiation-1(ID-1)led to inactivation of the AKT/mammalian target of rapamycin(m TOR)pathway,thus giving rise to autophagosome accumulation in PDAC cells.The magnitude of the increase in autophagosomes was sufficient to elicit ER stress-mediated apoptosis.Furthermore,ECON,as an autophagy inhibitor,exhibited synergistic effects with trametinib on PDAC.This study provides direct preclinical and experimental evidence for the therapeutic efficacy of ECON in PDAC treatment and reveals a mechanism whereby ECON inhibits PDAC growth. | Ningna Weng Siyuan Qin Jiayang Liu Xing Huang Jingwen Jiang Li Zhou Zhe Zhang Na Xie Kui Wang Ping Jin Maochao Luo Liyuan Peng Edouard C.Nice Ajay Goel Suxia Han Canhua Huang Qing Zhu | 2022 | Acta Pharmaceutica Sinica B2022，12，7： | 2 |
| 15 | Neoantigens:promising targets for cancer therapy显示文摘Recent advances in neoantigen research have accelerated the development and regulatory approval of tumor immunotherapies,including cancer vaccines,adoptive cell therapy and antibody-based therapies,especially for solid tumors.Neoantigens are newly formed antigens generated by tumor cells as a result of various tumor-specific alterations,such as genomic mutation,dysregulated RNA splicing,disordered post-translational modification,and integrated viral open reading frames.Neoantigens are recognized as non-self and trigger an immune response that is not subject to central and peripheral tolerance.The quick identification and prediction of tumor-specific neoantigens have been made possible by the advanced development of next-generation sequencing and bioinformatic technologies.Compared to tumor-associated antigens,the highly immunogenic and tumor-specific neoantigens provide emerging targets for personalized cancer immunotherapies,and serve as prospective predictors for tumor survival prognosis and immune checkpoint blockade responses.The development of cancer therapies will be aided by understanding the mechanism underlying neoantigen-induced anti-tumor immune response and by streamlining the process of neoantigen-based immunotherapies.This review provides an overview on the identification and characterization of neoantigens and outlines the clinical applications of prospective immunotherapeutic strategies based on neoantigens.We also explore their current status,inherent challenges,and clinical translation potential. | Na Xie Guobo Shen Wei Gao Zhao Huang Canhua Huang Li Fu | 2023 | Signal Transduction and Targeted Therapy2023，8，2： | 2 |
| 16 | From purines to purinergic signalling:molecular functions and human diseases显示文摘Purines and their derivatives,most notably adenosine and ATP,are the key molecules controlling intracellular energy homoeostasis and nucleotide synthesis.Besides,these purines support,as chemical messengers,purinergic transmission throughout tissues and species.Purines act as endogenous ligands that bind to and activate plasmalemmal purinoceptors,which mediate extracellular communication referred to as“purinergic signalling”.Purinergic signalling is cross-linked with other transmitter networks to coordinate numerous aspects of cell behaviour such as proliferation,differentiation,migration,apoptosis and other physiological processes critical for the proper function of organisms.Pathological deregulation of purinergic signalling contributes to various diseases including neurodegeneration,rheumatic immune diseases,inflammation,and cancer.Particularly,gout is one of the most prevalent purine-related disease caused by purine metabolism disorder and consequent hyperuricemia.Compelling evidence indicates that purinoceptors are potential therapeutic targets,with specific purinergic agonists and antagonists demonstrating prominent therapeutic potential.Furthermore,dietary and herbal interventions help to restore and balance purine metabolism,thus addressing the importance of a healthy lifestyle in the prevention and relief of human disorders.Profound understanding of molecular mechanisms of purinergic signalling provides new and exciting insights into the treatment of human diseases. | Zhao Huang Na Xie Peter Illes Francesco Di Virgilio Henning Ulrich Alexey Semyanov Alexei Verkhratsky Beata Sperlagh Shu-Guang Yu Canhua Huang Yong Tang | 2021 | Signal Transduction and Targeted Therapy2021，6，5： | 1 |
| 17 | Experiment study of flow in a vortex drop shaft 显示文摘 | Zhao Canhua David Z Z SUN Shuangke | 2006 | Journal of Hydraulic Engineerning2006，132，1： | 1 |
| 18 | Moire-pattern-modulated electronic structures in Sb_(2)Te_(3)/graphene heterostructure显示文摘Moire superlattice has recently been found in topological insulators,which can lead to periodic modulation on the electronic structure.In this work,we report the low-temperature scanning tunneling microscopy study of Sb_(2)Te_(3) films grown on graphitized 4H-SiC.We find that substrate temperature can strongly influence the rotation angles between Sb_(2)Te_(3) film and graphene substrate.Three kinds of moire patterns are observed at the first quintuple layer Sb_(2)Te_(3) film under different substrate temperatures.One shows complicated patterns with a rotation angle of nearly 0°relative to the substrate,another just exhibits simple 1 ×1 structure with a rotation angle of 30°.Other rotation angle like 8.2°is observed at higher substrate temperature as well,which is relatively rare.Comparison of the d//dV curves from Sb_(2)Te_(3) films with different moire patterns indicates that the superstructure can offer degrees of freedom in tailoring electronic structure.This work may stimulate the further study on the moire modulation to the electronic properties of topological insulators. | Yin Yin Guanyong Wang Chen Liu Haili Huang Jiayi Chen Jiaying Liu Dandan Guan Shiyong Wang Yaoyii Li Canhua Liu Hao Zheng Jinfeng Jia | 2022 | Nano Research2022，15，2： | 1 |
| 19 | Determination of deoxynivalenol (DON) and its derivatives: Current status of analytical methods显示文摘 | Ran Ran Canhua Wang Zheng Han Aibo Wu Dabing Zhang Jianxin Shi | 2013 | Food Control2013，，1： | 1 |
| 20 | The metabolic switch and its regulation in cancer cells显示文摘The primary features of cancer are maintained via intrinsically modified metabolic activity, which is characterized by enhanced nutrient supply, energy production, and biosynthetic activity to synthesize a variety of macromolecular components during each passage through the cell cycle. This metabolic shift in transformed cells, as compared with non-proliferating cells, in-volves aberrant activation of aerobic glycolysis, de novo lipid biosynthesis and glutamine-dependent anaplerosis to fuel robust cell growth and proliferation. Here, we discuss the unique metabolic characteristics of cancer, the constitutive regulation of metabolism through a variety of signal transduction pathways and/or enzymes involved in metabolic reprogramming in cancer cells, and their implications in cancer diagnosis and therapy. | ZHOU ShengTao, HUANG CanHua & WEI YuQuan State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China | 2010 | Science China(Life Sciences)2010，53，8： | 1 |
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