Galectins: Multitask signaling molecules linking fibroblast, endothelial and immune cell programs in the tumor microenvironment

被引:50
作者
Elola, Maria T. [1 ]
Ferragut, Fatima [1 ]
Mendez-Huergo, Santiago P. [2 ]
Croci, Diego O. [2 ,3 ]
Bracalente, Candelaria [1 ,5 ]
Rabinovich, Gabriel A. [2 ,4 ]
机构
[1] Univ Buenos Aires, Fac Farm & Bioquim, UBA CONICET, Inst Quim & Fisicoquim Biol Prof Dr Alejandro Pal, C1113, Buenos Aires, DF, Argentina
[2] Consejo Nacl Invest Cient & Tecn, IBYME, Lab Inmunopatol, Vuelta Obligado 2490,C1428, Buenos Aires, DF, Argentina
[3] Univ Nacl Cuyo, CONICET, Fac Exactas & Nat, Inst Histol & Embriol Dr Mario H Burgos IHEM,Lab, Mendoza, Argentina
[4] Univ Buenos Aires, Fac Ciencias Exactas & Nat, Dept Quim Biol, C1428, Buenos Aires, DF, Argentina
[5] Univ Manchester, CRUK Manchester Inst, Mol Oncol Grp, Wilmslow Rd, Manchester M20 4BX, Lancs, England
关键词
Galectins; Tumor microenvironment; Fibroblasts; Endothelial cells; Immune cells; BREAST-CANCER; STROMAL FIBROBLASTS; STELLATE CELLS; UP-REGULATION; T-CELLS; DIFFERENTIAL EXPRESSION; CHEMOKINE PRODUCTION; DERMAL FIBROBLASTS; CLASSICAL HODGKIN; GENE-EXPRESSION;
D O I
10.1016/j.cellimm.2018.03.008
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Tumor cells corrupt surrounding normal cells instructing them to support proliferative, pro-angiogenic and immunosuppressive networks that favor tumorigenesis and metastasis. This dynamic cross-talk is sustained by a range of intracellular signals and extracellular mediators produced by both tumoral and non-tumoral cells. Galectins-whether secreted or intracellularly expressed- play central roles in the tumorigenic process by delivering regulatory signals that contribute to reprogram fibroblasts, endothelial and immune cell programs. Through glycosylation-dependent or independent mechanisms, these endogenous lectins control a variety of cellular events leading to tumor cell proliferation, survival, migration, inflammation, angiogenesis and immune escape. Here we discuss the role of galectin-driven pathways, particularly those activated in non-tumoral stromal cells, in modulating tumor progression.
引用
收藏
页码:34 / 45
页数:12
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