Document Type
Article
Publication Date
8-11-2016
Abstract
The tumor microenvironment is a heterogeneous population of cells consisting of the tumor bulk plus supporting cells. It is becoming increasingly evident that these supporting cells are recruited by cancer cells from nearby endogenous host stroma and promote events such as tumor angiogenesis, proliferation, invasion, and metastasis, as well as mediate mechanisms of therapeutic resistance. In addition, recruited stromal cells range in type and include vascular endothelial cells, pericytes, adipocytes, fibroblasts, and bone-marrow mesenchymal stromal cells. During normal wound healing and inflammatory processes, local stromal cells change their phenotype to become that of reactive stroma. Under certain conditions, however, tumor cells can co-opt these reactive stromal cells and further transition them into tumor-associated stromal cells (TASCs). These TASCs express higher levels of proteins, including alpha-smooth muscle actin, fibroblast activating protein, and matrix metalloproteinases, compared with their normal, non-reactive counterparts. TASCs are also known to secrete many pro-tumorigenic factors, including IL-6, IL-8, stromal-derived factor-1 alpha, vascular endothelial growth factor, tenascin-C, and matrix metalloproteinases, among others, which recruit additional tumor and pro-tumorigenic cells to the developing microenvironment. Here, we review the current literature pertaining to the origins of recruited host stroma, contributions toward tumor progression, tumor-associated stromal cells, and mechanisms of crosstalk between endogenous host stroma and tumor cells.
Recommended Citation
Bussard, Karen M.; Mutkus, Lysette; Stumpf, Kristina; Gomez-Manzano, Candelaria; and Marini, Frank C., "Tumor-associated stromal cells as key contributors to the tumor microenvironment." (2016). Department of Cancer Biology Faculty Papers. Paper 95.
https://jdc.jefferson.edu/cbfp/95
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
PubMed ID
27515302
Comments
This article has been peer reviewed. It is the author’s final published version in Breast Cancer Research
Volume 18, Issue 1, August 2016, Article number 84.
The published version is available at DOI: 10.1186/s13058-016-0740-2. Copyright © Bussard et al.