Chemoresistance and the self-maintaining tumor microenvironment
File(s)cancers-10-00471.pdf (3.46 MB)
Published version
Author(s)
Yeldag, Gulcen
Rice, Alistair
Del Rio Hernandez, armando
Type
Journal Article
Abstract
The progression of cancer is associated with alterations in the tumor microenvironment, including changes in extracellular matrix (ECM) composition, matrix rigidity, hypervascularization, hypoxia, and paracrine factors. One key malignant phenotype of cancer cells is their ability to resist chemotherapeutics, and elements of the ECM can promote chemoresistance in cancer cells through a variety of signaling pathways, inducing changes in gene expression and protein activity that allow resistance. Furthermore, the ECM is maintained as an environment that facilitates chemoresistance, since its constitution modulates the phenotype of cancer-associated cells, which themselves affect the microenvironment. In this review, we discuss how the properties of the tumor microenvironment promote chemoresistance in cancer cells, and the interplay between these external stimuli. We focus on both the response of cancer cells to the external environment, as well as the maintenance of the external environment, and how a chemoresistant phenotype emerges from the complex signaling network present.
Date Issued
2018-11-28
Date Acceptance
2018-11-27
Citation
Cancers, 2018, 10 (12)
ISSN
2072-6694
Publisher
MDPI AG
Journal / Book Title
Cancers
Volume
10
Issue
12
Copyright Statement
© 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access
article distributed under the terms and conditions of the Creative Commons Attribution
(CC BY) license (http://creativecommons.org/licenses/by/4.0/).
article distributed under the terms and conditions of the Creative Commons Attribution
(CC BY) license (http://creativecommons.org/licenses/by/4.0/).
Sponsor
Commission of the European Communities
Grant Number
282051
Subjects
Science & Technology
Life Sciences & Biomedicine
Oncology
chemoresistance
ECM
fibrosis
hypoxia
mechanosignaling
paracrine
hypervascularization
cancer stem cells
EPITHELIAL-MESENCHYMAL TRANSITION
CANCER-ASSOCIATED FIBROBLASTS
GROWTH-FACTOR-BETA
INTERSTITIAL FLUID PRESSURE
NF-KAPPA-B
HYPOXIA-INDUCIBLE FACTOR-1-ALPHA
ACTIVATED PROTEIN-KINASE
EXTRACELLULAR-MATRIX
BREAST-CANCER
TGF-BETA
Publication Status
Published