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cancer metabolism and tumor microenvironment:fostering each other?

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Science China(Life Sciences) 2022年第2期65卷 236-279页

作者： 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 Obstetrics&Gynecology Hospital of Fudan University State Key Laboratory of Genetic EngineeringFudan UniversityShanghai 200438China State Key Laboratory of Cell Biology Center for Excellence in Molecular Cell ScienceChinese Academy of SciencesShanghai 200031China Molecular and Cell Biology Lab Institutes of Biomedical Sciences and School of Life SciencesFudan UniversityShanghai 200032China Zhejiang Provincial Key Laboratory of Pancreatic Disease The First Affiliated Hospitaland Institute of Translational MedicineZhejiang University School of MedicineHangzhou 310029China West China School of Basic Medical Sciences&Forensic Medicine Sichuan Universityand State Key Laboratory of Biotherapy and Cancer CenterWest China Hospitaland Collaborative Innovation Center for BiotherapyChengdu 610041China Department of Biochemistry and Molecular Cell Biology Shanghai Key Laboratory of Tumor Microenvironment and InflammationShanghai Jiao Tong University School of MedicineShanghai 200025China Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research CenterSun Yat-Sen Memorial HospitalSun Yat-Sen UniversityGuangzhou 510120China School of Life Science and Technology ShanghaiTech UniversityShanghai 201210China CAS Centre for Excellence in Cell and Molecular Biology the CAS Key Laboratory of Innate Immunity and Chronic DiseaseSchool of Basic Medical SciencesDivision of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefei 230027China School of Medicine Institutes for Life SciencesSouth China University of TechnologyGuangzhou 510006China Tsinghua University School of Life Sciences and Tsinghua-Peking Center for Life SciencesBeijing 100084China

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.

关键词： cancer metabolism cancer microenvironment epigenetics cancer immunology

The role of N-glycosylation in cancer

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Acta Pharmaceutica Sinica B 2024年第3期14卷 1098-1110页

作者： Yu Lin David M.Lubman Department of Surgery University of Michigan Medical CenterAnn ArborMI 48109USA

Despite advances in understanding the development and progression of cancer in recent years,there remains a lack of comprehensive characterization of the cancer glycoproteome.Glycoproteins play an important role in medicine and are involved in various human disease conditions including cancer.Glycan-moieties participate in fundamental cancer processes like cell signaling,invasion,angiogenesis,and metastasis.Aberrant N-glycosylation significantly impacts cancer processes and targeted therapies in clinic.Therefore,understanding N-glycosylation in a tumor is essential for comprehending disease progression and discovering anti-cancer targets and biomarkers for therapy monitoring and diagnosis.This review presents the fundamental process of protein N-glycosylation and summarizes glycosylation changes in tumor cells,including increased terminal sialylation,N-glycan branching,and corefucosylation.Also,the role of N-glycosylation in tumor signaling pathways,migration,and metabolism are discussed.Glycoproteins and glycopeptides as potential biomarkers for early detection of cancer based on site specificity have been introduced.Collectively,understanding and exploring the cancer glycoproteome,along with its role in medicine,implication in cancer and other human diseases,highlights the significance of N-glycosylation in tumor processes,necessitating further research for potential anticancer targets and biomarkers.

关键词： N-Glycosylated proteins cancer signaling cancer angiogenesis cancer metabolism cancer biomarkers

Aberrant LETM1 elevation dysregulates mitochondrial functions and energy metabolism and promotes lung metastasis in osteosarcoma

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Genes & Diseases 2024年第3期11卷 368-384页

作者： Yulu Shi Quan Kang Hong Zhou Xiaohan Yue Yang Bi Qing Luo Stem Cell Biology and Therapy Laboratory The Children's Hospital of Chongqing Medical UniversityNational Clinical Research Center for Child Health and DisordersMinistry of Education Key Laboratory of Child Development and DisordersChongqing Key Laboratory of PediatricsChongqing 400014China Department of Pediatric Surgery The Children's Hospital of Chongqing Medical UniversityChongqing 400014China

Osteosarcoma is a differentiation-deficient disease,and despite the unique advan-tages and great potential of differentiation therapy,there are only a few known differentia-tion inducers,and little research has been done on their targets.Cell differentiation is associated with an increase in mitochondrial content and activity.The metabolism of some tu-mor cells is characterized by impaired oxidative phosphorylation,as well as up-regulation of aerobic glycolysis and pentose phosphate pathways.Leucine-containing zipper and EF-hand transmembrane protein 1(LETM1)is involved in the maintenance of mitochondrial morphology and is closely associated with tumorigenesis and progression,as well as cancer cell stemness.We found that MG63 and 143B osteosarcoma cells overexpress LETM1 and exhibit abnormalities in mitochondrial structure and function.Knockdown of LETM1 partially restored the mitochon-drial structure and function,inhibited the pentose phosphate pathway,promoted oxidative phosphorylation,and led to osteogenic differentiation.It also inhibited spheroid cell forma-tion,proliferation,migration,and invasion in an in vitro model.When LETM1 was knocked down in vivo,there was reduced tumor formation and lung metastasis.These data suggest that mitochondria are aberrant in LETM1-overexpressing osteosarcoma cells,and knockdown of LETM1 partially restores the mitochondrial structure and function,inhibits the pentose phosphate pathway,promotes oxidative phosphorylation,and increases osteogenic differentiation,thereby reducing malignant biological behavior of the cells.

关键词： cancer metabolism Differentiation LETM1 Osteosarcoma Stemness

Coherent Raman scattering imaging of lipid metabolism in cancer

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Journal of Innovative Optical Health Sciences 2023年第3期16卷 3-12页

作者： Shuo Zhang Yexuan He Shuhua Yue Key Laboratory of Biomechanics and Mechanobiology(Beihang University) Ministry of EducationInstitute of Medical PhotonicsBeijing Advanced Innovation Center for Biomedical EngineeringSchool of Biological Science and Medical EngineeringBeihang UniversityBeijing 100083P.R.China MoE Key Laboratory for Biomedical Photonics Wuhan National Laboratory for Optoelectronics-Huazhong University of Science and TechnologyWuhan 430074P.R.China

cancer cells dysregulate lipid metabolism to accelerate energy production and biomolecule synthesis for rapid growth.Lipid metabolism is highly dynamic and intrinsically heterogeneous at the single cell level.Although°uorescence microscopy has been commonly used for cancer research,bulky°uorescent probes can hardly label small lipid molecules without perturbing their biological activities.Such a challenge can be overcome by coherent Raman scattering(CRS)microscopy,which is capable of chemically selective,highly sensitive,submicron resolution and high-speed imaging of lipid molecules in single live cells without any labeling.Recently developed hyperspectral and multiplex CRS microscopy enables quantitative mapping of various lipid metabolites in situ.Further incorporation of CRS microscopy with Raman tags greatly increases molecular selectivity based on the distinct Raman peaks well separated from the endogenous cellular background.Owing to these unique advantages,CRS microscopy sheds new insights into the role of lipid metabolism in cancer development and progression.This review focuses on the latest applications of CRS microscopy in the study of lipid metabolism in cancer.

关键词： Coherent Raman scattering microscopy cancer metabolism lipid metabolism

The emerging role and targetability of the TCA cycle in cancer metabolism

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Protein & Cell 2018年第2期9卷 216-237页

作者： Nicole M. Anderson Patrick Mucka Joseph G. Kern Hui Feng Abramson Family cancer Research Institute University of Pennsylvania Philadelphia PA 19104-6160 USA Perelman School of Medicine at the University of Pennsylvania Philadelphia PA 19104 USA Departments of Pharmacology and Medicine The Center for Cancer Research Section of Hematology and Medical Oncology Boston University School of Medicine Boston MA 02118 USA Program in Biomedical Sciences Boston University School of Medicine Boston MA 02118 USA

The tricarboxylic acid （TCA） cycle is a central route for oxidative phosphorylation in cells, and fulfills their bioenergetic, biosynthetic, and redox balance require- ments. Despite early dogma that cancer cells bypass the TCA cycle and primarily utilize aerobic glycolysis, emerging evidence demonstrates that certain cancer cells, especially those with deregulated oncogene and tumor suppressor expression, rely heavily on the TCA cycle for energy production and macromolecule synthesis. As the field progresses, the importance of aberrant TCA cycle function in tumorigenesis and the potentials of applying small molecule inhibitors to perturb the enhanced cycle function for cancer treatment start to evolve. In this review, we summarize current knowledge about the fuels feeding the cycle, effects of oncogenes and tumor suppressors on fuel and cycle usage, common genetic alterations and deregulation of cycle enzymes, and potential therapeutic opportunities for targeting the TCA cycle in cancer cells. With the application of advanced technology and in vivo model organism studies, it is our hope that studies of this previously overlooked biochemical hub will provide fresh insights into cancer metabolism and tumorigenesis, subsequently revealing vulnerabilities for thera- peutic interventions in various cancer types.

关键词： glutaminolysis the TCA cycle cancer metabolism glycolysis

Aerobic glycolysis and high level of lactate in cancer metabolism and microenvironment

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Genes & Diseases 2017年第1期4卷 25-27页

作者： Bo Jiang Department of Oncology Avis General HospitalBeijingChina

Metabolic abnormalities is a hallmark of cancer.About 100 years ago,Nobel laureate Otto Heinrich Warburg first described high rate of glycolysis in cancer cells.Recently more and more novel opinions about cancer metabolism supplement to this hypothesis,consist of glucose uptake,lactic acid generation and secretion,acidification of the microenvironment and cancer immune evasion.Here we briefly review metabolic pathways generating lactate,and discuss the function of higher lactic acid in cancer microenvironments.

关键词： Aerobic glycolysis cancer metabolism Glucose metabolism Immune escape Lactate

New insights into molecules and pathways of cancer metabolism and therapeutic implications

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cancer Communications 2021年第1期41卷 16-36页

作者： Zhenye Tang Zhenhua Xu Xiao Zhu Jinfang Zhang Southern Marine Science and Engineering Guangdong Laboratory Zhanjiang the Marine Medical Research Institute of Guangdong ZhanjiangGuangdong Medical UniversityZhanjiangGuangdong 524023P.R.China Southern Marine Science and Engineering Guangdong Laboratory(Zhanjiang) ZhanjiangGuangdong 524023P.R.China Center for cancer and Immunology Brain Tumor InstituteChildren’s National Health SystemWashingtonDC 20010USA The Key Lab of Zhanjiang for R&D Marine Microbial Resources in the Beibu Gulf Rim Guangdong Medical UniversityZhanjiangGuangdong 524023P.R.China The Marine Biomedical Research Institute of Guangdong Zhanjiang Guangdong Medical UniversityZhanjiangGuangdong 524023P.R.China Lingnan Medical Research Center the First Affiliated Hospital of Guangzhou University of Chinese Medicinethe First Clinical Medical CollegeGuangzhou University of Chinese MedicineGuangzhouGuangdong 510405P.R.China

cancer cells are abnormal cells that can reproduce and regenerate rapidly.They are characterized by unlimited proliferation,transformation and migration,and can destroy normal cells.To meet the needs for cell proliferation and migration,tumor cells acquire molecular materials and energy through unusual metabolic pathways as their metabolism is more vigorous than that of normal cells.Multiple carcinogenic signaling pathways eventually converge to regulate three major metabolic pathways in tumor cells,including glucose,lipid,and amino acid metabolism.The distinct metabolic signatures of cancer cells reflect that metabolic changes are indispensable for the genesis and development of tumor cells.In this review,we report the unique metabolic alterations in tumor cells which occur through various signaling axes,and present various modalities available for cancer diagnosis and clinical therapy.We further provide suggestions for the development of anti-tumor therapeutic drugs.

关键词： cancer metabolism metabolic pathway metabolomic profiling therapeutic implication

LncRNA-mediated posttranslational modifications and reprogramming of energy metabolism in cancer

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cancer Communications 2021年第2期41卷 109-120页

作者： Yue-Tao Tan Jin-Fei Lin Ting Li Jia-Jun Li Rui-Hua Xu Huai-Qiang Ju Department of Medical Oncology Sun Yat-sen University Cancer CenterState Key Laboratory of Oncology in South ChinaCollaborative Innovation Center for Cancer MedicineGuangzhouGuangdong 510060P.R.China Research Unit of Precision Diagnosis and Treatment for Gastrointestinal cancer Chinese Academy of Medical SciencesGuangzhouGuangdong 510060P.R.China

Altered metabolism is a hallmark of cancer,and the reprogramming of energy metabolism has historically been considered a general phenomenon of tumors.It is well recognized that long noncoding RNAs(lncRNAs)regulate energy metabolism in cancer.However,lncRNA-mediated posttranslational modifications and metabolic reprogramming are unclear at present.In this review,we summarized the current understanding of the interactions between the alterations in cancer-associated energy metabolism and the lncRNA-mediated posttranslational modifications of metabolic enzymes,transcription factors,and other proteins involved in metabolic pathways.In addition,we discuss the mechanisms through which these interactions contribute to tumor initiation and progression,and the key roles and clinical significance of functional lncRNAs.We believe that an in-depth understanding of lncRNA-mediated cancer metabolic reprogramming can help to identify cellular vulnerabilities that can be exploited for cancer diagnosis and therapy.

关键词： cancer metabolism enzyme long noncoding RNA metabolic reprogramming posttranslational modification

cancer metabolism in gastrointestinal cancer

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Journal of cancer Metastasis and Treatment 2015年第1期1卷 172-182页

作者： Hiroshi Sawayama Nobutomo Miyanari Hideo Baba Department of Surgery National Hospital Organization Kumamoto Medical Center1-5 NinomaruKumamoto 860-0008Japan Department of Gastroenterological Surgery Graduate School of Medical SciencesKumamoto University1-1-1 HonjoKumamoto 860-8556Japan.

cancer cells exhibit altered glucose metabolism,mitochondrial dysfunction,anaerobic glycolysis and upregulation of the pentose phosphate pathway(PPP).Recent genetic and metabolic analyses have provided insights into the molecular mechanisms of genes that are involved in the alteration of cancer metabolism and tumorigenesis.Hypoxic induced factor 1 regulates the reciprocal relationship between glycolysis and oxidative phosphorylation,and p53 also modulates the balance between the glycolytic pathway and oxidative phosphorylation.Mitochondria function in cancer differs from that in normal cells owing to mutations of mitochondrial DNA and alterations of metabolism.Overexpression of transcription factors,metabolite transporters and glycolytic enzymes is observed and associated with poor prognosis,and it may be associated with chemoradiotherapy resistance in multiple cancer cell types.The PPP plays a critical role in regulating cancer cell growth by supplying cells with ribose-5-phosphate and nicotinamide adenine dinucleotide phosphate for detoxifi cation of intra-cellular reactive oxygen species(ROS),reductive biosynthesis and ribose biogenesis.ROS levels increase during carcinogenesis owing to metabolic aberrations.This review discusses alterations of mitochondrial metabolism,anaerobic glycolysis,the PPP and control of ROS levels by the endogenous anti-oxidant system in cancer,as well as the novel small molecules targeting these enzymes or transporters that exert anti-proliferative effects.

关键词： Anti-oxidants cancer metabolism mitochondria pentose phosphate pathway reactive oxygen species Warburg effect