Tumor microenvironment and angiogenesis

被引:158
作者
Nyberg, Pia [1 ]
Salo, Tuula [1 ]
Kalluri, Raghu [2 ,3 ,4 ]
机构
[1] Univ Oulu, Inst Dent, Dept Diagnost & Oral Med, FIN-90014 Oulu, Finland
[2] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Ctr Matrix Biol, Boston, MA USA
[3] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA USA
[4] Harvard MIT Div Hlth Sci & Technol, Boston, MA USA
关键词
extracellular matrix; fibroblast; immune cell; integrin; microenvironment; tumor angiogenesis; review;
D O I
10.2741/3173
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The tumor microenvironment is a mixture of extracellular matrix molecules, tumor cells, endothelial cells, fibroblasts and immune cells. Tumor growth and metastasis formation are dependent on the growth of blood vessels into the tumor mass. The tumor microenvironment contributes to this pathological angiogenic process. The extracellular matrix and basement membranes are a source for endogenous angiogenesis inhibitors, such as endostatin. On the other hand, many extracellular matrix molecules can promote angiogenesis by stabilizing blood vessels and sequestering pro-angiogenic growth factors. The majority of stromal cells in carcinomas are fibroblasts. Carcinoma-associated fibroblasts show a distinct phenotype from normal fibroblasts. The mechanisms how the tumor-associated fibroblasts regulate angiogenesis are not fully known, but they are suggested to be an important source for growth factors and cytokines recruiting endothelial cells. The immune cells, particularly macrophages and neutrophils are another source for angiogenesis-regulating chemokines, growth factors and proteases. Taken together, the tumor microenvironment is a complex unorganized tissue of various cell types and extracellular matrix that can regulate the pathological angiogenic switch.
引用
收藏
页码:6537 / 6553
页数:17
相关论文
共 184 条
[41]   ANGIOGENESIS IN CANCER, VASCULAR, RHEUMATOID AND OTHER DISEASE [J].
FOLKMAN, J .
NATURE MEDICINE, 1995, 1 (01) :27-31
[42]   Opinion - Angiogenesis: an organizing principle for drug discovery? [J].
Folkman, Judah .
NATURE REVIEWS DRUG DISCOVERY, 2007, 6 (04) :273-286
[43]  
FOLMAN J, 1971, NEW ENGL J MED, V285, P1182
[44]   Expression of CD44v3 protein in human endothelial cells in vitro and in tumoral microvessels in vivo [J].
Forster-Horváth, C ;
Mészáros, L ;
Rásó, E ;
Döme, B ;
Ladányi, A ;
Morini, M ;
Albini, A ;
Tímár, J .
MICROVASCULAR RESEARCH, 2004, 68 (02) :110-118
[45]   DEFINITION OF 2 ANGIOGENIC PATHWAYS BY DISTINCT ALPHA(V) INTEGRINS [J].
FRIEDLANDER, M ;
BROOKS, PC ;
SHAFFER, RW ;
KINCAID, CM ;
VARNER, JA ;
CHERESH, DA .
SCIENCE, 1995, 270 (5241) :1500-1502
[46]   Tumor induction of VEGF promoter activity in stromal cells [J].
Fukumura, D ;
Xavier, R ;
Sugiura, T ;
Chen, Y ;
Park, EC ;
Lu, NF ;
Selig, M ;
Nielsen, G ;
Taksir, T ;
Jain, RK ;
Seed, B .
CELL, 1998, 94 (06) :715-725
[47]   GROWTH AND DIFFERENTIATION CHARACTERISTICS OF TRANSFORMED KERATINOCYTES FROM MOUSE AND HUMAN-SKIN INVITRO AND INVIVO [J].
FUSENIG, NE ;
BREITKREUTZ, D ;
DZARLIEVA, RT ;
BOUKAMP, P ;
BOHNERT, A ;
TILGEN, W .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1983, 81 (01) :S168-S175
[48]   An amino-bisphosphonate targets MMP-9-expressing macrophages and angiogenesis to impair cervical carcinogenesis [J].
Giraudo, E ;
Inoue, M ;
Hanahan, D .
JOURNAL OF CLINICAL INVESTIGATION, 2004, 114 (05) :623-633
[49]   A TUMOR SUPPRESSOR-DEPENDENT INHIBITOR OF ANGIOGENESIS IS IMMUNOLOGICALLY AND FUNCTIONALLY INDISTINGUISHABLE FROM A FRAGMENT OF THROMBOSPONDIN [J].
GOOD, DJ ;
POLVERINI, PJ ;
RASTINEJAD, F ;
LEBEAU, MM ;
LEMONS, RS ;
FRAZIER, WA ;
BOUCK, NP .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (17) :6624-6628
[50]   Hypoxia-mediated selection of cells with diminished apoptotic potential in solid tumours [J].
Graeber, TG ;
Osmanian, C ;
Jacks, T ;
Housman, DE ;
Koch, CJ ;
Lowe, SW ;
Giaccia, AJ .
NATURE, 1996, 379 (6560) :88-91