• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

肿瘤-基质相互作用在乳腺癌中的代谢意义。

Metabolic implication of tumor:stroma crosstalk in breast cancer.

机构信息

Department of Experimental and Clinical Biomedical Sciences, University of Florence, viale GB Morgagni 50, Florence, I-50134, Italy.

出版信息

J Mol Med (Berl). 2014 Feb;92(2):117-26. doi: 10.1007/s00109-014-1124-7. Epub 2014 Jan 24.

DOI:10.1007/s00109-014-1124-7
PMID:24458539
Abstract

The metabolic properties of cancer cells significantly differ from those of normal cells. In particular, cancer cells are largely dependent on aerobic glycolysis, a phenomenon that has been exploited clinically by using labelled glucose for positron emission tomography imaging. Importantly, cancer-associated alterations in metabolism are not merely due to the resulting response to cell proliferation and survival. Indeed, direct metabolic regulation could be driven by tumor oncogenes and/or suppressors, as demonstrated in several solid tumors, including breast cancer. Despite the fact that most breast cancer studies have focused on the intrinsic characteristics of breast tumor cells, it is now widely accepted that tumor microenvironment plays an important role in defining and reprogramming cancer cell metabolism. Tumor:stroma crosstalk, as well as inflammatory cues, concurs to outlining the cancer metabolism, impact on cancer aggressiveness and ultimately on patient survival and therapeutic responses. The aim of this review is to (i) gather the most recent data regarding the metabolic alterations in breast cancer, (ii) describe the role of tumor microenvironment in breast cancer cell metabolic reprogramming, and (iii) contemplate how targeting metabolic pathways aberrantly activated in breast cancer could help current therapeutic regimens.

摘要

癌细胞的代谢特性与正常细胞有显著差异。特别是,癌细胞在很大程度上依赖于有氧糖酵解,这一现象已被临床应用于使用标记葡萄糖进行正电子发射断层扫描成像。重要的是,与癌症相关的代谢变化不仅仅是由于细胞增殖和存活的反应。事实上,正如在包括乳腺癌在内的几种实体瘤中所证明的那样,直接的代谢调节可能是由肿瘤致癌基因和/或抑癌基因驱动的。尽管大多数乳腺癌研究都集中在乳腺肿瘤细胞的内在特征上,但现在人们普遍认为肿瘤微环境在定义和重编程癌细胞代谢方面起着重要作用。肿瘤-基质相互作用以及炎症线索共同描绘了癌症代谢,影响癌症侵袭性,并最终影响患者的生存和治疗反应。本综述的目的是:(i)收集有关乳腺癌代谢改变的最新数据,(ii)描述肿瘤微环境在乳腺癌细胞代谢重编程中的作用,以及(iii)思考靶向乳腺癌中异常激活的代谢途径如何帮助当前的治疗方案。

相似文献

1
Metabolic implication of tumor:stroma crosstalk in breast cancer.肿瘤-基质相互作用在乳腺癌中的代谢意义。
J Mol Med (Berl). 2014 Feb;92(2):117-26. doi: 10.1007/s00109-014-1124-7. Epub 2014 Jan 24.
2
Metabolic reprogramming of cancer-associated fibroblasts by TGF-β drives tumor growth: connecting TGF-β signaling with "Warburg-like" cancer metabolism and L-lactate production.转化生长因子-β(TGF-β)重塑肿瘤相关成纤维细胞的代谢以促进肿瘤生长:将 TGF-β 信号与“Warburg-like”肿瘤代谢和 L-乳酸生成联系起来。
Cell Cycle. 2012 Aug 15;11(16):3019-35. doi: 10.4161/cc.21384. Epub 2012 Aug 9.
3
Impact of tumor microenvironment and epithelial phenotypes on metabolism in breast cancer.肿瘤微环境和上皮表型对乳腺癌代谢的影响。
Clin Cancer Res. 2013 Feb 1;19(3):571-85. doi: 10.1158/1078-0432.CCR-12-2123. Epub 2012 Dec 12.
4
Understanding the Warburg effect and the prognostic value of stromal caveolin-1 as a marker of a lethal tumor microenvironment.了解沃伯格效应和基质窖蛋白-1作为致命肿瘤微环境标志物的预后价值。
Breast Cancer Res. 2011 Jul 8;13(4):213. doi: 10.1186/bcr2892.
5
Metabolic crosstalk in the breast cancer microenvironment.乳腺癌微环境中的代谢串扰。
Eur J Cancer. 2019 Nov;121:154-171. doi: 10.1016/j.ejca.2019.09.002. Epub 2019 Sep 30.
6
Tumor microenvironment and metabolic synergy in breast cancers: critical importance of mitochondrial fuels and function.肿瘤微环境与乳腺癌的代谢协同作用:线粒体燃料和功能的关键重要性。
Semin Oncol. 2014 Apr;41(2):195-216. doi: 10.1053/j.seminoncol.2014.03.002. Epub 2014 Mar 5.
7
Stromal cells in tumor microenvironment and breast cancer.肿瘤微环境中的基质细胞与乳腺癌。
Cancer Metastasis Rev. 2013 Jun;32(1-2):303-15. doi: 10.1007/s10555-012-9415-3.
8
Nutrient Exploitation within the Tumor-Stroma Metabolic Crosstalk.肿瘤-基质代谢串扰中的营养物质利用
Trends Cancer. 2016 Dec;2(12):736-746. doi: 10.1016/j.trecan.2016.11.001. Epub 2016 Dec 6.
9
Tumor stroma interaction is mediated by monocarboxylate metabolism.肿瘤与基质的相互作用是由单羧酸代谢介导的。
Exp Cell Res. 2017 Mar 1;352(1):20-33. doi: 10.1016/j.yexcr.2017.01.013. Epub 2017 Jan 26.
10
Integrated Bioinformatics Approach Reveals Crosstalk Between Tumor Stroma and Peripheral Blood Mononuclear Cells in Breast Cancer.整合生物信息学方法揭示乳腺癌中肿瘤基质与外周血单个核细胞之间的相互作用。
Asian Pac J Cancer Prev. 2016;17(3):1003-8. doi: 10.7314/apjcp.2016.17.3.1003.

引用本文的文献

1
Distinguishing metastatic triple-negative breast cancer from nonmetastatic breast cancer using second harmonic generation imaging and resonance Raman spectroscopy.使用二次谐波成像和共振拉曼光谱区分转移性三阴性乳腺癌与非转移性乳腺癌。
J Biophotonics. 2020 Jul;13(7):e202000005. doi: 10.1002/jbio.202000005. Epub 2020 Apr 20.
2
Screening of immunosuppressive factors for biomarkers of breast cancer malignancy phenotypes and subtype-specific targeted therapy.筛选免疫抑制因子作为乳腺癌恶性表型生物标志物及亚型特异性靶向治疗
PeerJ. 2019 Jun 27;7:e7197. doi: 10.7717/peerj.7197. eCollection 2019.
3
Eugenol inhibits oxidative phosphorylation and fatty acid oxidation via downregulation of c-Myc/PGC-1β/ERRα signaling pathway in MCF10A-ras cells.

本文引用的文献

1
Glucose deprivation increases monocarboxylate transporter 1 (MCT1) expression and MCT1-dependent tumor cell migration.葡萄糖剥夺会增加单羧酸转运蛋白 1(MCT1)的表达和依赖 MCT1 的肿瘤细胞迁移。
Oncogene. 2014 Jul 31;33(31):4060-8. doi: 10.1038/onc.2013.454. Epub 2013 Oct 28.
2
A novel model of dormancy for bone metastatic breast cancer cells.骨转移乳腺癌细胞休眠的新模型。
Cancer Res. 2013 Dec 1;73(23):6886-99. doi: 10.1158/0008-5472.CAN-13-0991. Epub 2013 Oct 21.
3
PKM2 isoform-specific deletion reveals a differential requirement for pyruvate kinase in tumor cells.
丁香酚通过下调 MCF10A-ras 细胞中 c-Myc/PGC-1β/ERRα 信号通路抑制氧化磷酸化和脂肪酸氧化。
Sci Rep. 2017 Oct 10;7(1):12920. doi: 10.1038/s41598-017-13505-x.
4
Characterization of the Tumor Microenvironment and Tumor-Stroma Interaction by Non-invasive Preclinical Imaging.通过非侵入性临床前成像对肿瘤微环境和肿瘤-基质相互作用进行表征。
Front Oncol. 2017 Jan 31;7:3. doi: 10.3389/fonc.2017.00003. eCollection 2017.
5
Tumor stroma interaction is mediated by monocarboxylate metabolism.肿瘤与基质的相互作用是由单羧酸代谢介导的。
Exp Cell Res. 2017 Mar 1;352(1):20-33. doi: 10.1016/j.yexcr.2017.01.013. Epub 2017 Jan 26.
6
Ultraconserved long non-coding RNA uc.63 in breast cancer.乳腺癌中的超保守长链非编码RNA uc.63
Oncotarget. 2017 May 30;8(22):35669-35680. doi: 10.18632/oncotarget.10572.
7
Targeting hypoxic response for cancer therapy.靶向缺氧反应用于癌症治疗。
Oncotarget. 2016 Mar 22;7(12):13464-78. doi: 10.18632/oncotarget.7229.
8
Hypoxia-Activated Prodrug TH-302 Targets Hypoxic Bone Marrow Niches in Preclinical Leukemia Models.缺氧激活前药TH-302在临床前白血病模型中靶向缺氧骨髓微环境。
Clin Cancer Res. 2016 Apr 1;22(7):1687-98. doi: 10.1158/1078-0432.CCR-14-3378. Epub 2015 Nov 24.
9
Targeting stromal-induced pyruvate kinase M2 nuclear translocation impairs oxphos and prostate cancer metastatic spread.靶向基质诱导的丙酮酸激酶M2核转位会损害氧化磷酸化和前列腺癌转移扩散。
Oncotarget. 2015 Sep 15;6(27):24061-74. doi: 10.18632/oncotarget.4448.
10
Modeling cancer metabolism on a genome scale.在基因组规模上模拟癌症代谢。
Mol Syst Biol. 2015 Jun 30;11(6):817. doi: 10.15252/msb.20145307.
PKM2 同工型特异性缺失揭示了丙酮酸激酶在肿瘤细胞中的不同需求。
Cell. 2013 Oct 10;155(2):397-409. doi: 10.1016/j.cell.2013.09.025.
4
New perspective for an old antidiabetic drug: metformin as anticancer agent.一种老降糖药的新视角:二甲双胍作为抗癌药物
Cancer Treat Res. 2014;159:355-76. doi: 10.1007/978-3-642-38007-5_21.
5
Metformin reverses multidrug resistance and epithelial-mesenchymal transition (EMT) via activating AMP-activated protein kinase (AMPK) in human breast cancer cells.二甲双胍通过激活人乳腺癌细胞中的 AMP 激活的蛋白激酶(AMPK)逆转多药耐药和上皮-间充质转化(EMT)。
Mol Cell Biochem. 2014 Jan;386(1-2):63-71. doi: 10.1007/s11010-013-1845-x. Epub 2013 Oct 6.
6
Influence of tumour micro-environment heterogeneity on therapeutic response.肿瘤微环境异质性对治疗反应的影响。
Nature. 2013 Sep 19;501(7467):346-54. doi: 10.1038/nature12626.
7
Loss of caveolin-1 and gain of MCT4 expression in the tumor stroma: key events in the progression from an in situ to an invasive breast carcinoma.肿瘤基质中 caveolin-1 的缺失和 MCT4 的表达增加:原位乳腺癌向浸润性乳腺癌进展的关键事件。
Cell Cycle. 2013 Aug 15;12(16):2684-90. doi: 10.4161/cc.25794. Epub 2013 Jul 29.
8
Pyruvate kinase M2: regulatory circuits and potential for therapeutic intervention.丙酮酸激酶M2:调控机制及治疗干预潜力
Curr Pharm Des. 2014;20(15):2595-606. doi: 10.2174/13816128113199990484.
9
Cancer-associated fibroblasts and M2-polarized macrophages synergize during prostate carcinoma progression.癌相关成纤维细胞和 M2 极化的巨噬细胞在前列腺癌进展过程中协同作用。
Oncogene. 2014 May 8;33(19):2423-31. doi: 10.1038/onc.2013.191. Epub 2013 Jun 3.
10
GDNF-RET signaling in ER-positive breast cancers is a key determinant of response and resistance to aromatase inhibitors.GDNF-RET 信号在 ER 阳性乳腺癌中是对芳香化酶抑制剂的反应和耐药的关键决定因素。
Cancer Res. 2013 Jun 15;73(12):3783-95. doi: 10.1158/0008-5472.CAN-12-4265. Epub 2013 May 6.