2018
DOI: 10.1016/j.bbcan.2018.09.002
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Dynamic matrisome: ECM remodeling factors licensing cancer progression and metastasis

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Cited by 106 publications
(87 citation statements)
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References 390 publications
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“…In addition, treatment of a KPC/CAF coculture with DON in vitro showed that there was extensive downregulation in the expression of ECM proteases such as MMP12, MMP7, and MMP8 ( Figure 5). These proteases are involved in dynamic remodeling of the ECM during tumor progression, specifically regulating metastasis (63). Recent studies have shown that amino acid-mediated metabolic crosstalk between CAFs and tumor epithelial cells affects the biophysical as well as biological properties of the tumor (64).…”
Section: Resultsmentioning
confidence: 99%
“…In addition, treatment of a KPC/CAF coculture with DON in vitro showed that there was extensive downregulation in the expression of ECM proteases such as MMP12, MMP7, and MMP8 ( Figure 5). These proteases are involved in dynamic remodeling of the ECM during tumor progression, specifically regulating metastasis (63). Recent studies have shown that amino acid-mediated metabolic crosstalk between CAFs and tumor epithelial cells affects the biophysical as well as biological properties of the tumor (64).…”
Section: Resultsmentioning
confidence: 99%
“…Herein, cancer would be an illustrative example of such a "cell development-metabolism synchronization". Indeed, whereas cancer represents a status in which ECM remodeling is required and observed [56][57][58], cancer cells and the tumor microenvironment have specific metabolic profiles and unique bioenergetic properties in different form noncancer cells [59,60]. Interestingly, SPARC was suggested to play a homeostasis-regulatory role in cancer.…”
Section: Sparc: Metabolics and Homeostasismentioning
confidence: 99%
“…Regarding cellular component, a noticeable enriched term of DEGs was extracellular matrix. Intimate and complex communications between tumor cells and the ECM have been established and this result emphasized the roles of DEGs in HNSCC progression [22][23][24]. What is more, KEGG analysis results suggested these genes showed enrichment in cytokine-cytokine receptor interaction, cell adhesion molecules (CAMs), B cell receptor signaling pathway, and Toll-like receptor signaling pathway, all were functional processes involved in HNSCC pathogenesis.…”
Section: Discussionmentioning
confidence: 83%