Cancer-associated fibroblasts that restrain cancer progression: Hypotheses and perspectives.
Animals
Cancer-Associated Fibroblasts
/ metabolism
Cell Transformation, Neoplastic
/ genetics
Drug Resistance, Neoplasm
/ genetics
Extracellular Matrix
/ genetics
Heterografts
Humans
Mesenchymal Stem Cells
/ metabolism
Mice
Neoplasms
/ genetics
Neovascularization, Pathologic
/ genetics
Pancreatic Stellate Cells
/ metabolism
Tumor Microenvironment
/ genetics
Meflin
cancer-restraining cancer-associated fibroblasts
fibrosis
mesenchymal stem/stromal cells
tumor microenvironment
Journal
Cancer science
ISSN: 1349-7006
Titre abrégé: Cancer Sci
Pays: England
ID NLM: 101168776
Informations de publication
Date de publication:
Apr 2020
Apr 2020
Historique:
received:
02
11
2019
revised:
26
01
2020
accepted:
02
02
2020
pubmed:
16
2
2020
medline:
23
4
2020
entrez:
16
2
2020
Statut:
ppublish
Résumé
The roles of cancer-associated fibroblasts (CAF) in the progression of various types of cancers are well established. CAF promote cancer progression through pleiotropic mechanisms, including the secretion of soluble factors and extracellular matrix, physical interactions with cancer cells, and the regulation of angiogenesis, immunity and metabolism. Their contribution to therapeutic resistance is also well appreciated. Therefore, CAF have been considered as a therapeutic target in cancer. However, recent studies in autochthonous pancreatic cancer models suggest that specific subset(s) of CAF exhibit cancer-restraining roles, indicating that CAF are functionally and molecularly heterogeneous, which is supported by recent single-cell transcriptome analyses. While cancer-promoting CAF (pCAF) have been extensively studied, the nature and specific marker(s) of cancer-restraining CAF (rCAF) have remained uncharacterized. Interestingly, a recent study provided insight into the nature of rCAF and suggested that they may share molecular properties with pancreatic stellate cells (PSC) and mesenchymal stem/stromal cells (MSC). Complicating this finding is that PSC and MSC have been shown to promote the formation of a tumor-permissive and tumor-promoting environment in xenograft tumor models. However, these cells undergo significant transcriptional and epigenetic changes during ex vivo culture, which confounds the interpretation of experimental results based on the use of cultured cells. In this short review, we describe recent studies and hypotheses on the identity of rCAF and discuss their analogy to fibroblasts that suppress fibrosis in fibrotic diseases. Finally, we discuss how these findings can be exploited to develop novel anticancer therapies in the future.
Identifiants
pubmed: 32060987
doi: 10.1111/cas.14346
pmc: PMC7156845
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1047-1057Subventions
Organisme : Ministry of Education, Culture, Sports, Science and Technology of Japan
ID : 26221304
Organisme : Ministry of Education, Culture, Sports, Science and Technology of Japan
ID : 18H02638
Organisme : Japan Agency for Medical Research and Development, Core Research for Evolutional Science and Technology
ID : 19gm0810007h0104
Organisme : Japan Agency for Medical Research and Development, Core Research for Evolutional Science and Technology
ID : 19gm1210008s0101
Organisme : Project for Cancer Research and Therapeutic Evolution (P-CREATE) from AMED
ID : 19cm0106332h0002
Informations de copyright
© 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
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