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Article: Therapeutic targeting of the crosstalk between cancer-associated fibroblasts and cancer stem cells

TitleTherapeutic targeting of the crosstalk between cancer-associated fibroblasts and cancer stem cells
Authors
KeywordsCAFs
CSCs
cancer stemness
therapeutic resistance
cancer therapy
Issue Date2019
PublisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajcr.us
Citation
American Journal of Cancer Research, 2019, v. 9 n. 9, p. 1889-1904 How to Cite?
AbstractCancer-associated fibroblasts (CAFs) play critical roles in cancer progression and treatment failure. CAFs display extreme phenotypic heterogeneity and functional diversity. Some subpopulations of CAFs have the ability to reconstitute cancer stemness by promoting the expansion of cancer stem cells (CSCs) or by inducing the generation of CSCs from differentiated cancer cells. CAFs regulate cancer stemness in different types of solid tumors by activating a wide array of CSC-related signaling by secreting proteins and exosomes. As feedback, the CSCs can also induce the proliferation and further activation of CAFs to promote their CSC-supporting activities, thus completing the loop of CAF-CSC crosstalk. Current research on targeting CAF-CSC crosstalk could be classified into (i) specific depletion of CAF subpopulations that have CSC-supporting activities and (ii) targeting molecular signaling in CAF-CSC crosstalk, such as the IL6/STAT3, TGF-β/SDF-1/PI3K, WNT/β-catenin, HGF/cMET and SHH/Hh pathways. Strategies targeting CAF-CSC crosstalk may open new avenues for overcoming cancer progression and therapeutic resistance.
Persistent Identifierhttp://hdl.handle.net/10722/284546
ISSN
2023 Impact Factor: 3.6
2019 SCImago Journal Rankings: 1.562
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHuang, TX-
dc.contributor.authorGuan, XY-
dc.contributor.authorFu, L-
dc.date.accessioned2020-08-07T08:59:10Z-
dc.date.available2020-08-07T08:59:10Z-
dc.date.issued2019-
dc.identifier.citationAmerican Journal of Cancer Research, 2019, v. 9 n. 9, p. 1889-1904-
dc.identifier.issn2156-6976-
dc.identifier.urihttp://hdl.handle.net/10722/284546-
dc.description.abstractCancer-associated fibroblasts (CAFs) play critical roles in cancer progression and treatment failure. CAFs display extreme phenotypic heterogeneity and functional diversity. Some subpopulations of CAFs have the ability to reconstitute cancer stemness by promoting the expansion of cancer stem cells (CSCs) or by inducing the generation of CSCs from differentiated cancer cells. CAFs regulate cancer stemness in different types of solid tumors by activating a wide array of CSC-related signaling by secreting proteins and exosomes. As feedback, the CSCs can also induce the proliferation and further activation of CAFs to promote their CSC-supporting activities, thus completing the loop of CAF-CSC crosstalk. Current research on targeting CAF-CSC crosstalk could be classified into (i) specific depletion of CAF subpopulations that have CSC-supporting activities and (ii) targeting molecular signaling in CAF-CSC crosstalk, such as the IL6/STAT3, TGF-β/SDF-1/PI3K, WNT/β-catenin, HGF/cMET and SHH/Hh pathways. Strategies targeting CAF-CSC crosstalk may open new avenues for overcoming cancer progression and therapeutic resistance.-
dc.languageeng-
dc.publisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajcr.us-
dc.relation.ispartofAmerican Journal of Cancer Research-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectCAFs-
dc.subjectCSCs-
dc.subjectcancer stemness-
dc.subjecttherapeutic resistance-
dc.subjectcancer therapy-
dc.titleTherapeutic targeting of the crosstalk between cancer-associated fibroblasts and cancer stem cells-
dc.typeArticle-
dc.identifier.emailGuan, XY: xyguan@hku.hk-
dc.identifier.authorityGuan, XY=rp00454-
dc.description.naturepublished_or_final_version-
dc.identifier.pmid31598393-
dc.identifier.pmcidPMC6780671-
dc.identifier.hkuros312297-
dc.identifier.volume9-
dc.identifier.issue9-
dc.identifier.spage1889-
dc.identifier.epage1904-
dc.identifier.isiWOS:000488234300003-
dc.publisher.placeUnited States-
dc.identifier.issnl2156-6976-

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