z-logo
open-access-imgOpen Access
Extracellular matrix guidance of autophagy: a mechanism regulating cancer growth
Author(s) -
Carolyn Chen,
Renato V. Iozzo
Publication year - 2022
Publication title -
open biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.078
H-Index - 53
ISSN - 2046-2441
DOI - 10.1098/rsob.210304
Subject(s) - autophagy , biology , microbiology and biotechnology , extracellular matrix , carcinogenesis , reprogramming , cancer cell , thrombospondin , angiogenesis , cancer , cancer research , matrix metalloproteinase , biochemistry , cell , genetics , apoptosis , metalloproteinase
The extracellular matrix (ECM) exists as a dynamic network of biophysical and biochemical factors that maintain tissue homeostasis. Given its sensitivity to changes in the intra- and extracellular space, the plasticity of the ECM can be pathological in driving disease through aberrant matrix remodelling. In particular, cancer uses the matrix for its proliferation, angiogenesis, cellular reprogramming and metastatic spread. An emerging field of matrix biology focuses on proteoglycans that regulate autophagy, an intracellular process that plays both critical and contextual roles in cancer. Here, we review the most prominent autophagic modulators from the matrix and the current understanding of the cellular pathways and signalling cascades that mechanistically drive their autophagic function. We then critically assess how their autophagic functions influence tumorigenesis, emphasizing the complexities and stage-dependent nature of this relationship in cancer. We highlight novel emerging data on immunoglobulin-containing and proline-rich receptor-1, heparanase and thrombospondin 1 in autophagy and cancer. Finally, we further discuss the pro- and anti-autophagic modulators originating from the ECM, as well as how these proteoglycans and other matrix constituents specifically influence cancer progression.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here