2003
DOI: 10.1038/sj.onc.1206887
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Expression profiling of epithelial plasticity in tumor progression

Abstract: Epithelial-to-mesenchymal transition (EMT), a switch of polarized epithelial cells to a migratory, fibroblastoid phenotype, is increasingly considered as an important event during malignant tumor progression and metastasis. To identify molecular players involved in EMT and metastasis, we performed expression profiling of a set of combined in vitro/in vivo cellular models, based on clonal, fully polarized mammary epithelial cells. Seven closely related cell pairs were used, which were modified by defined oncoge… Show more

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Cited by 273 publications
(240 citation statements)
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References 51 publications
(92 reference statements)
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“…19 GSEA revealed a significant overlap between the Fra-1-derived gene sets and the genes upregulated in EpRas cells upon TGF-β-induced EMT 21 (Table 1a). Genes associated with c-Myb 29 or with promoters occupied by Smad2/3, 30 two TFs connected to TGF-β and EMT, 31,32 were also enriched (Table 1b) Figure S6a, Figures 5a and b).…”
Section: Resultsmentioning
confidence: 99%
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“…19 GSEA revealed a significant overlap between the Fra-1-derived gene sets and the genes upregulated in EpRas cells upon TGF-β-induced EMT 21 (Table 1a). Genes associated with c-Myb 29 or with promoters occupied by Smad2/3, 30 two TFs connected to TGF-β and EMT, 31,32 were also enriched (Table 1b) Figure S6a, Figures 5a and b).…”
Section: Resultsmentioning
confidence: 99%
“…13,14 Ras and TGFβ cooperate to induce and stabilize a mesenchymal switch in EpH4 cells. 21,22,40 Unlike human breast cancer cells where upstream signalling kinases activation is required, 14,16 ectopic Fra-1 expression was sufficient for EMT and tumorigenesis in EpH4 cells. Moreover, Fra-1 increased TGFβ expression and production, similarly to c-Fos and unlike oncogenic Ras, 43 thus TGFβ treatment was not necessary for EMT in EpFra1 cells.…”
Section: Discussionmentioning
confidence: 99%
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“…The characteristic of EMT is that cells acquire mesenchymal cell markers (eg, N‐cadherin and vimentin) and lose epithelial cell markers (eg, E‐cadherin) 5, 6. EMT occurs during the progression of tumors of various origins, including prostate, breast, hepatic, gastric, pancreatic, and colorectal cancer 7, 8, 9, 10, 11, 12…”
Section: Introductionmentioning
confidence: 99%
“…[21][22][23] The accumulation of cytoplasmic b-catenin and its translocation to the nucleus has been associated with epithelial cell migration and invasion in various physiological and pathological processes including tumour progression. 21,[23][24][25][26] Several b-catenin/TCF target genes have now been identified. They pertain to various families of proteins including matrix metalloproteases, cytoskeletal proteins or angiogenic cytokines and chemokines (IL-8, MMP-7, MMP-14, CD44, cyclin D1, c-myc, claudin-1, vimentin, MMP26, VEGF.…”
mentioning
confidence: 99%