Relationship of VEGF/VEGFR with immune and cancer cells: staggering or forward?

被引:152
作者
Li, Yu -Ling [1 ]
Zhao, Hua [1 ,2 ]
Ren, Xiu-Bao [1 ,2 ]
机构
[1] Tianjin Med Univ, Canc Inst & Hosp, Dept Biotherapy, Natl Clin Res Ctr Canc, Tianjin 300060, Peoples R China
[2] Res Ctr Lung Canc, Key Lab Canc Immunol & Biotherapy, Tianjin 300060, Peoples R China
关键词
ENDOTHELIAL GROWTH-FACTOR; TUMOR-ASSOCIATED MACROPHAGES; REGULATORY T-CELLS; OVARIAN-CANCER; FACTOR RECEPTOR-3; VEGF-C; CLINICAL-SIGNIFICANCE; FACTOR EXPRESSION; DENDRITIC CELLS; CUTTING EDGE;
D O I
10.20892/j.issn.2095-3941.2015.0070
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Vascular endothelial growth factor (VEGF) is primarily known as a proangiogenic factor and is one of the most important growth and survival factors affecting the vascular endothelium. However, recent studies have shown that VEGF also plays a vital role in the immune environment. In addition to the traditional growth factor role of VEGF and VEGF receptors (VEGFRs), they have a complicated relationship with various immune cells. VEGF also reportedly inhibits the differentiation and function of immune cells during hematopoiesis. Dendritic cells (DCs), macrophages, and lymphocytes further express certain types of VEGF receptors. VEGF can be secreted as well by tumor cells through the autocrine pathway and can stimulate the function of cancer stemness. This review will provide a paradigm shift in our understanding of the role of VEGF/VEGFR signaling in the immune and cancer environment.
引用
收藏
页码:206 / 214
页数:9
相关论文
共 75 条
[1]   Migration of human monocytes in response to vascular endothelial growth factor (VEGF) is mediated via the VEGF receptor flt-1 [J].
Barleon, B ;
Sozzani, S ;
Zhou, D ;
Weich, HA ;
Mantovani, A ;
Marme, D .
BLOOD, 1996, 87 (08) :3336-3343
[2]   Cutting Edge: Vascular Endothelial Growth Factor-Mediated Signaling in Human CD45RO+ CD4+ T Cells Promotes Akt and ERK Activation and Costimulates IFN-γ Production [J].
Basu, Aninda ;
Hoerning, Andre ;
Datta, Dipak ;
Edelbauer, Monika ;
Stack, Maria P. ;
Calzadilla, Katiana ;
Pal, Soumitro ;
Briscoe, David M. .
JOURNAL OF IMMUNOLOGY, 2010, 184 (02) :545-549
[3]   A vascular niche and a VEGF-Nrp1 loop regulate the initiation and stemness of skin tumours [J].
Beck, Benjamin ;
Driessens, Gregory ;
Goossens, Steven ;
Youssef, Khalil Kass ;
Kuchnio, Anna ;
Caauwe, Amelie ;
Sotiropoulou, Panagiota A. ;
Loges, Sonja ;
Lapouge, Gaelle ;
Candi, Aurelie ;
Mascre, Guilhem ;
Drogat, Benjamin ;
Dekoninck, Sophie ;
Haigh, Jody J. ;
Carmeliet, Peter ;
Blanpain, Cedric .
NATURE, 2011, 478 (7369) :399-+
[4]   Tumorigenesis and the angiogenic switch [J].
Bergers, G ;
Benjamin, LE .
NATURE REVIEWS CANCER, 2003, 3 (06) :401-410
[5]   INDIRECT ANGIOGENIC CYTOKINES UP-REGULATE VEGF AND BFGF GENE-EXPRESSION IN VASCULAR SMOOTH-MUSCLE CELLS, WHEREAS HYPOXIA UP-REGULATES VEGF EXPRESSION ONLY [J].
BROGI, E ;
WU, TG ;
NAMIKI, A ;
ISNER, JM .
CIRCULATION, 1994, 90 (02) :649-652
[6]   Lung vascular endothelial growth factor expression induces local myeloid dendritic cell activation [J].
Chapoval, Svetlana P. ;
Lee, Chun Geun ;
Tang, Chuyan ;
Keegan, Achsah D. ;
Cohn, Lauren ;
Bottomly, Kim ;
Elias, Jack A. .
CLINICAL IMMUNOLOGY, 2009, 132 (03) :371-384
[7]   Vascular endothelial growth factor, FLT-1, and FLK-1 analysis in a pancreatic cancer tissue microarray [J].
Chung, GG ;
Yoon, HH ;
Zerkowski, MP ;
Ghosh, S ;
Thomas, L ;
Harigopal, M ;
Charette, LA ;
Salem, RR ;
Camp, RL ;
Rimm, DL ;
Burtness, BA .
CANCER, 2006, 106 (08) :1677-1684
[8]  
Cursiefen C, 2002, INVEST OPHTH VIS SCI, V43, P2127
[9]   Vascular endothelial growth factor (VEGF)-C signaling through FLT-4 (VEGFR-3) mediates leukemic cell proliferation, survival, and resistance to chemotherapy [J].
Dias, S ;
Choy, M ;
Alitalo, K ;
Rafii, S .
BLOOD, 2002, 99 (06) :2179-2184
[10]   Differential roles of vascular endothelial growth factor receptors 1 and 2 in dendritic cell differentiation [J].
Dikov, MM ;
Ohm, JE ;
Ray, N ;
Tchekneva, EE ;
Burlison, J ;
Moghanaki, D ;
Nadaf, S ;
Carbone, DP .
JOURNAL OF IMMUNOLOGY, 2005, 174 (01) :215-222