Macrophages and Metabolism in the Tumor Microenvironment

被引：1337

作者：

Vitale, Ilio ^{[1
,2
,3
]}

Manic, Gwenola ^{[4
]}

Coussens, Lisa M. ^{[5
]}

Kroemer, Guido ^{[6
,7
,8
,9
,10
,11
,12
,13
]}

Galluzzi, Lorenzo ^{[6
,14
,15
,16
]}

机构：

[1] Univ Roma Tor Vergata, Dept Biol, Rome, Italy

[2] IIGM, Turin, Italy

[3] IRCCS, Candiolo Canc Inst FPO, Candiolo, Italy

[4] IRCSS Regina Elena Natl Canc Inst, Rome, Italy

[5] Oregon Hlth & Sci Univ, Knight Canc Inst, Dept Cell Dev & Canc Biol, Portland, OR 97201 USA

[6] Univ Paris 05, Paris, France

[7] Univ Paris 06, Paris, France

[8] Ctr Rech Cordeliers, Equipe 11 Labellisee Ligue Natl Canc, Paris, France

[9] INSERM, F-U1138 Paris, France

[10] Metabol & Cell Biol Platforms, Gustave Roussy Canc Campus, Villejuif, France

[11] Hop Europeen Georges Pompidou, AP HP, Pole Biol, Paris, France

[12] Chinese Acad Sci, Suzhou Inst Syst Med, Suzhou, Peoples R China

[13] Karolinska Univ Hosp, Dept Womens & Childrens Hlth, Stockholm, Sweden

[14] Weill Cornell Med Coll, Dept Radiat Oncol, New York, NY USA

[15] Sandra & Edward Meyer Canc Ctr, New York, NY USA

[16] Yale Univ, Sch Med, Dept Dermatol, New Haven, CT 06510 USA

来源：

CELL METABOLISM | 2019年 / 30卷 / 01期

基金：

美国国家卫生研究院;

关键词：

CANCER-ASSOCIATED FIBROBLASTS; T-CELL METABOLISM; SUPPRESSOR-CELLS; M2; MACROPHAGES; MYELOID CELLS; IMMUNE CELLS; THERAPEUTIC RESISTANCE; AEROBIC GLYCOLYSIS; O-GLCNACYLATION; GENE-EXPRESSION;

D O I：

10.1016/j.cmet.2019.06.001

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Tumor-associated macrophages (TAMs) constitute a plastic and heterogeneous cell population of the tumor microenvironment (TME) that can account for up to 50% of some solid neoplasms. Most often, TAMs support disease progression and resistance to therapy by providing malignant cells with trophic and nutritional support. However, TAMs can mediate antineoplastic effects, especially in response to pharmacological agcnts that boost their phagocytic and oxidative functions. Thus, TAMs and their impact on the overall metabolic profile of the TME have a major influence on tumor progression and resistance to therapy, de facto constituting promising targets for the development of novel anticancer agents. Here, we discuss the metabolic circuitries whereby TAMs condition the TME to support tumor growth and how such pathways can be therapeutically targeted.

引用

页码：36 / 50

页数：15

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