Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 Apr 19;11(4):dmm029447.
doi: 10.1242/dmm.029447.

A peek into cancer-associated fibroblasts: origins, functions and translational impact

Affiliations
Review

A peek into cancer-associated fibroblasts: origins, functions and translational impact

Valerie S LeBleu et al. Dis Model Mech. .

Abstract

In malignant tumors, cancer cells adapt to grow within their host tissue. As a cancer progresses, an accompanying host stromal response evolves within and around the nascent tumor. Among the host stromal constituents associated with the tumor are cancer-associated fibroblasts, a highly abundant and heterogeneous population of cells of mesenchymal lineage. Although it is known that fibroblasts are present from the tumor's inception to the end-stage metastatic spread, their precise functional role in cancer is not fully understood. It has been suggested that cancer-associated fibroblasts play a key role in modulating the behavior of cancer cells, in part by promoting tumor growth, but evolving data also argue for their antitumor actions. Taken together, this suggests a putative bimodal function for cancer-associated fibroblasts in oncogenesis. As illustrated in this Review and its accompanying poster, cancer-associated fibroblasts are a dynamic component of the tumor microenvironment that orchestrates the interplay between the cancer cells and the host stromal response. Understanding the complexity of the relationship between cancer cells and cancer-associated fibroblasts could offer insights into the regulation of tumor progression and control of cancer.

Keywords: Cancer; Fibroblasts; Heterogeneity.

PubMed Disclaimer

References

    1. Albrengues J., Bertero T., Grasset E., Bonan S., Maiel M., Bourget I., Philippe C., Serrano C. H., Benamar S., Croce O. et al. (2015). Epigenetic switch drives the conversion of fibroblasts into proinvasive cancer-associated fibroblasts. 6 10.1038/ncomms10204 - DOI - PMC - PubMed
    1. Alexander J. and Cukierman E. (2016). Stromal dynamic reciprocity in cancer: intricacies of fibroblastic-ECM interactions. 42, 80-93. 10.1016/j.ceb.2016.05.002 - DOI - PMC - PubMed
    1. Anderberg C., Li H., Fredriksson L., Andrae J., Betsholtz C., Li X., Eriksson U. and Pietras K. (2009). Paracrine signaling by platelet-derived growth factor-CC promotes tumor growth by recruitment of cancer-associated fibroblasts. 69, 369-378. 10.1158/0008-5472.CAN-08-2724 - DOI - PMC - PubMed
    1. Armulik A., Genové G. and Betsholtz C. (2011). Pericytes: developmental, physiological, and pathological perspectives, problems, and promises. 21, 193-215. 10.1016/j.devcel.2011.07.001 - DOI - PubMed
    1. Augsten M. (2014). Cancer-associated fibroblasts as another polarized cell type of the tumor microenvironment. 4, 62 10.3389/fonc.2014.00062 - DOI - PMC - PubMed

Publication types

MeSH terms