Dual Role of Fibroblasts Educated by Tumour in Cancer Behavior and Therapeutic Perspectives
Metadata
Show full item recordEditorial
MDPI
Materia
Tumour microenvironment Cancer-associated fibroblast Cancer cell Magnification Inflammation Metastasis
Date
2022-12-08Referencia bibliográfica
Toledo, B... [et al.]. Dual Role of Fibroblasts Educated by Tumour in Cancer Behavior and Therapeutic Perspectives. Int. J. Mol. Sci. 2022, 23, 15576. [https://doi.org/10.3390/ijms232415576]
Sponsorship
Consejería de Economía, Conocimiento, Empresas y Universidad de la Junta de Andalucía and European Regional Development Fund (ERDF), ref. P18-FR-2470,; Ministry of Science, Innovation and Universities (ref. RTI2018-101309-B-C22); Chair “Doctors Galera-Requena in cancer stem cell research” (CMC-CTS963)Abstract
Tumours are complex systems with dynamic interactions between tumour cells, nontumour
cells, and extracellular components that comprise the tumour microenvironment (TME). The
majority of TME’s cells are cancer-associated fibroblasts (CAFs), which are crucial in extracellular
matrix (ECM) construction, tumour metabolism, immunology, adaptive chemoresistance, and tumour
cell motility. CAF subtypes have been identified based on the expression of protein markers. CAFs
may act as promoters or suppressors in tumour cells depending on a variety of factors, including
cancer stage. Indeed, CAFs have been shown to promote tumour growth, survival and spread, and
secretome changes, but they can also slow tumourigenesis at an early stage through mechanisms that
are still poorly understood. Stromal–cancer interactions are governed by a variety of soluble factors
that determine the outcome of the tumourigenic process. Cancer cells release factors that enhance the
ability of fibroblasts to secrete multiple tumour-promoting chemokines, acting on malignant cells
to promote proliferation, migration, and invasion. This crosstalk between CAFs and tumour cells
has given new prominence to the stromal cells, from being considered as mere physical support to
becoming key players in the tumour process. Here, we focus on the concept of cancer as a non-healing
wound and the relevance of chronic inflammation to tumour initiation. In addition, we review CAFs
heterogeneous origins and markers together with the potential therapeutic implications of CAFs
“re-education” and/or targeting tumour progression inhibition.