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Semin Cancer Biol. 2014 Apr;25:15-22. doi: 10.1016/j.semcancer.2013.12.008. Epub 2014 Jan 7.

TGF-beta in CAF-mediated tumor growth and metastasis.

Author information

1
Oncology Department, Institute for Research in Biomedicine, 08028 Barcelona, Spain. Electronic address: alexandre.calon@irbbarcelona.org.
2
Oncology Department, Institute for Research in Biomedicine, 08028 Barcelona, Spain.
3
Oncology Department, Institute for Research in Biomedicine, 08028 Barcelona, Spain; Institució Catalana de Recerca i Estudis Avançats (ICREA), 08010 Barcelona, Spain. Electronic address: eduard.batlle@irbbarcelona.org.

Abstract

TGF-beta signaling is one of the major pathways controlling cell and tissue behavior not only in homeostasis but also in disease. During tumorigenesis TGF-beta orchestrated processes are key due to its dual role as tumor suppressor and tumor promoter. Important functions of this pathway have been described in a context-dependent manner both in epithelial cancer cells and in the tumor microenvironment during tumor progression. Carcinoma-associated fibroblasts (CAFs) are one of the most abundant stromal cell types in virtually all solid tumors. CAFs favor malignant progression by providing cancer cells with proliferative, migratory, survival and invasive capacities. A complex network of signaling pathways underlying their tumor-promoting properties is beginning to take shape. In this review, we examine current evidence on the emerging mechanisms involving TGF-beta in CAF-mediated cancer progression, and discuss their potential as therapeutic targets.

KEYWORDS:

Cancer-associated fibroblast; Metastasis; Stroma; TGF-beta; Tumor microenvironment

PMID:
24412104
DOI:
10.1016/j.semcancer.2013.12.008
[Indexed for MEDLINE]

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