肿瘤代谢研究新进展

doi:10.3760/cma.j.issn.1673-422X.2015.04.010

国际肿瘤学杂志 ›› 2015, Vol. 42 ›› Issue (4): 277-280.doi: 10.3760/cma.j.issn.1673-422X.2015.04.010

肿瘤代谢研究新进展

200025上海交通大学医学院病理生理系细胞分化与凋亡教育部重点实验室(郭文正、邓炯)；上海市肿瘤微环境与炎症重点实验室,上海市胸科医院转化医学研究中心（邓炯）

出版日期:2015-04-08 发布日期:2015-04-22
通讯作者: 邓炯，Email: jiongdeng@shsmu.edu.cn
基金资助:
国家自然科学基金(81071923、91129303)

Research progress of cancer metabolism

Department of Pathophysiology, Key laboratory of Cell Differentiation and Apoptosis of Education Minister, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China

Online:2015-04-08 Published:2015-04-22
Contact: Deng Jiong, Email: jiongdeng@shsmu.edu.cn

摘要/Abstract

摘要： 与正常细胞相比，肿瘤细胞因其基因或者表观遗传的改变，导致许多代谢通路发生紊乱。正常细胞发生恶化过程中，不仅糖代谢通路发生异常，线粒体生物合成、氨基酸代谢、脂代谢等其他代谢通路也会发生变化。这些代谢变化对肿瘤的发生发展以及临床靶向治疗具有重要的意义。

关键词: 肿瘤, 代谢

Abstract: Compared to normal counterparts, cancer cells exhibit metabolic changes owing to both genetic and epigenetic alterations. Some abnormal alterations happen in tumor cells including glycolysis, mitochondrial biogenesis, glutaminolysis and lipid synthesis. These metabolic changes have great significance to development of tumor and clinical targeted therapies.

Key words: Neoplasms, Metabolism

郭文正；邓炯. 肿瘤代谢研究新进展[J]. 国际肿瘤学杂志, 2015, 42(4): 277-280.

GUO Wen-Zheng-；Deng-Jiong. Research progress of cancer metabolism[J]. Journal of International Oncology, 2015, 42(4): 277-280.

参考文献

［1］ Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation［J］. Cell, 2011, 144(5): 646674. ［2］ Vander Heiden MG, Cantley LC, Thompson CB. Understanding the Warburg effect: the metabolic requirements of cell proliferation［J］. Science, 2009, 324(5930): 10291033. ［3］ Jones RG, Thompson CB. Tumor suppressors and cell metabolism: a recipe for cancer growth［J］. Genes Dev, 2009, 23(5): 537548. ［4］ Ying H, Kimmelman AC, Lyssiotis CA, et al. Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism［J］. Cell, 2012, 149(3): 656670. ［5］ Engelman JA. Targeting PI3K signalling in cancer: opportunities, challenges andlimitations［J］. Nat Rev Cancer, 2009, 9(8): 550562 . ［6］ Dong C, Yuan T, Wu Y, et al. Loss of FBP1 by Snailmediated repression provides metabolic advantages in basallike breast cancer［J］. Cancer cell, 2013, 23(3): 316331. ［7］ Yang L, Xie M, Yang M, et al. PKM2 regulates the Warburg effect and promotes HMGB1 release in sepsis［J］. Nat Commun, 2014, 5:4436. ［8］ Yang W, Xia Y, Hawke D, et al. PKM2 phosphorylates histone H3 and promotes gene transcription and tumorigenesis［J］. Cell, 2012, 150(4): 685696. ［9］ MartinezOutschoorn UE, Prisco M, Ertel A, et al. Ketones and lactate increase cancer cell "stemness," driving recurrence, metastasis and poor clinical outcome in breast cancer: achieving personalized medicine via MetaboloGenomics［J］. Cell cycle, 2011, 10(8): 12711286. ［10］ Riganti C, Gazzano E, Polimeni M, et al. The pentose phosphate pathway: an antioxidant defense and a crossroad in tumor cell fate［J］. Free Radic Bio Med, 2012, 53(3): 421436. ［11］ Hartmannsberger D, Mack B, Eggert C, et al. Transketolaselike protein 1 confers resistance to serum withdrawal in vitro［J］. Cancer Lett, 2011, 300(1): 2029. ［12］ Ren F, Wu H, Lei Y, et al. Quantitative proteomics identification of phosphoglycerate mutase 1 as a novel therapeutic target in hepatocellular carcinoma［J］. Mol Cancer, 2010, 9: 81. ［13］ Hitosugi T, Zhou L, Elf S, et al. Phosphoglycerate mutase 1 coordinates glycolysis and biosynthesis to promote tumor growth［J］. Cancer cell, 2012, 22(5): 585600. ［14］ Galtieri A, Tellone E, Ficarra S, et al. Resveratrol treatment induces redox stress in red blood cells: a possible role of caspase 3 in metabolism and anion transport［J］. Bio Chem, 2010, 391(9): 10571065. ［15］ Pan S, World CJ, Kovacs CJ, et al. Glucose 6phosphate dehydrogenase is regulated through cSrcmediated tyrosine phosphorylation in endothelial cells［J］. Arterioscler Thromb Vasc Biol, 2009, 29(6): 895901. ［16］ Possemato R, Marks KM, Shaul YD, et al. Functional genomics reveal that the serine synthesis pathway is essential in breast cancer［J］. Nature, 2011, 476(7360): 346350. ［17］ Yamamoto T, Takano N, Ishiwata K, et al. Reduced methylation of PFKFB3 in cancer cells shunts glucose towards the pentose phosphate pathway［J］. Nat Commun, 2014, 5: 3480. ［18］ Yalcin A, Clem BF, ImbertFernandez Y, et al. 6Phosphofructo2kinase (PFKFB3) promotes cell cycle progression and suppresses apoptosis via Cdk1mediated phosphorylation of p27［J］. Cell Death Dis, 2014, 5:e1337. ［19］ Wallace DC. Mitochondria and cancer［J］. Nat Rev Cancer, 2012, 12(10): 685698. ［20］ Dang CV. Glutaminolysis: supplying carbon or nitrogen or both for cancer cells?［J］. Cell cycle, 2010, 9(19): 38843886. ［21］ Sandulache VC, Ow TJ, Pickering CR, et al. Glucose, not glutamine, is the dominant energy source required for proliferation and survival of head and neck squamous carcinoma cells［J］. Cancer, 2011, 117(13): 29262938. ［22］ Gao P, Tchernyshyov I, Chang TC, et al. cMyc suppression of miR23a/b enhances mitochondrial glutaminase expression and glutamine metabolism［J］. Nature, 2009, 458(7239): 762765. ［23］ Yuneva MO, Fan TW, Allen TD, et al. The metabolic profile of tumors depends on both the responsible genetic lesion and tissue type［J］. Cell Metab, 2012, 15(2): 157170. ［24］ Santos CR, Schulze A. Lipid metabolism in cancer［J］. FEBS J, 2012, 279(15): 26102623. ［25］ Furuta E, Pai SK, Zhan R, et al. Fatty acid synthase gene is upregulated by hypoxia via activation of Akt and sterol regulatory element binding protein1［J］. Cancer Res, 2008, 68(4): 10031011. ［26］ Wang JB, Erickson JW, Fuji R, et al. Targeting mitochondrial glutaminase activity inhibits oncogenic transformation［J］. Cancer cell, 2010, 18(3): 207219. ［27］ Israelsen WJ, Dayton TL, Davidson SM, et al. PKM2 isoformspecific deletion reveals a differential requirement for pyruvate kinase in tumor cells［J］. Cell, 2013, 155(2): 397409. ［28］ Le A, Cooper CR, Gouw AM, et al. Inhibition of lactate dehydrogenase A induces oxidative stress and inhibits tumor progression［J］. Proc Natl Acad Sci USA, 2010, 107(5): 20372042.

[1]	刘娜, 寇介丽, 杨枫, 刘桃桃, 李丹萍, 韩君蕊, 杨立洲. 血清miR-106b-5p、miR-760联合低剂量螺旋CT诊断早期肺癌的临床价值[J]. 国际肿瘤学杂志, 2024, 51(6): 321-325.
[2]	杨蜜, 别俊, 张加勇, 邓佳秀, 唐组阁, 卢俊. 局部晚期可切除食管癌新辅助治疗疗效及预后分析[J]. 国际肿瘤学杂志, 2024, 51(6): 332-337.
[3]	袁健, 黄燕华. Hp-IgG抗体联合血清DKK1、sB7-H3对早期胃癌的诊断价值[J]. 国际肿瘤学杂志, 2024, 51(6): 338-343.
[4]	陈红健, 张素青. 血清miR-24-3p、H2AFX与肝癌患者临床病理特征及术后复发的关系研究[J]. 国际肿瘤学杂志, 2024, 51(6): 344-349.
[5]	郭泽浩, 张俊旺. PFDN及其亚基在肿瘤发生发展中的作用[J]. 国际肿瘤学杂志, 2024, 51(6): 350-353.
[6]	张百红, 岳红云. 新作用机制的抗肿瘤药物进展[J]. 国际肿瘤学杂志, 2024, 51(6): 354-358.
[7]	许凤琳, 吴刚. EBV在鼻咽癌肿瘤免疫微环境和免疫治疗中的研究进展[J]. 国际肿瘤学杂志, 2024, 51(6): 359-363.
[8]	王盈, 刘楠, 郭兵. 抗体药物偶联物在转移性乳腺癌治疗中的研究进展[J]. 国际肿瘤学杂志, 2024, 51(6): 364-369.
[9]	张蕊, 褚衍六. 基于FIT与肠道菌群的结直肠癌风险评估模型的研究进展[J]. 国际肿瘤学杂志, 2024, 51(6): 370-375.
[10]	高凡, 王萍, 杜超, 褚衍六. 肠道菌群与结直肠癌非手术治疗的相关研究进展[J]. 国际肿瘤学杂志, 2024, 51(6): 376-381.
[11]	王丽, 刘志华, 杨伟洪, 蒋凤莲, 李全泳, 宋浩杰, 鞠文东. ROS1突变肺腺鳞癌合并脑梗死为主要表现的Trousseau综合征1例[J]. 国际肿瘤学杂志, 2024, 51(6): 382-384.
[12]	刘静, 刘芹, 黄梅. 基于SMOTE算法的食管癌放化疗患者肺部感染的预后模型构建[J]. 国际肿瘤学杂志, 2024, 51(5): 267-273.
[13]	杨琳, 路宁, 温华, 张明鑫, 朱琳. 炎症负荷指数与胃癌临床关系研究[J]. 国际肿瘤学杂志, 2024, 51(5): 274-279.
[14]	王俊毅, 洪楷彬, 纪荣佳, 陈大朝. 癌结节对结直肠癌根治性切除术后肝转移的影响[J]. 国际肿瘤学杂志, 2024, 51(5): 280-285.
[15]	张宁宁, 杨哲, 檀丽梅, 李振宁, 王迪, 魏永志. 宫颈细胞DNA倍体分析联合B7-H4和PKCδ对宫颈癌的诊断价值[J]. 国际肿瘤学杂志, 2024, 51(5): 286-291.

肿瘤代谢研究新进展

Research progress of cancer metabolism

PDF

可视化

摘要/Abstract

引用本文

使用本文

参考文献

相关文章 15

编辑推荐

Metrics

本文评价