Tumor-induced upregulation of Twist, Snail, and Slug represses the activity of the human VE-cadherin promoter

Lopez, Dayami; Niu, Guilian; Huber, Philippe; Carter, W. Bradford

doi:10.1016/j.abb.2008.11.016

Cited by 65 publications

(51 citation statements)

References 20 publications

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“…Sp1, TAL-1, and the ETS family of transcription factors bind to and enhance VE-cadherin promoter activity (49 -51). In contrast, Snail, Slug, and Twist transcription factors are responsible for the down-regulation of VE-cadherin promoter activity by binding to the E-box of the promoter region (26). The binding between these transcription factors and the human VE-cadherin promoter were shown in an in vitro system using EMSA (26).…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, Snail, Slug, and Twist transcription factors are responsible for the down-regulation of VE-cadherin promoter activity by binding to the E-box of the promoter region (26). The binding between these transcription factors and the human VE-cadherin promoter were shown in an in vitro system using EMSA (26). Thus, whether Snail, Slug, or Twist can bind to human VE-cadherin promoter within a natural chromatin cellular context and whether the binding of these transcription factors can directly regulate VE-cadherin mRNA and protein levels still remain unknown.…”

Section: Discussionmentioning

confidence: 99%

“…8E). Previous study using the electrophoretic mobility shift assay (EMSA) showed that Snail could bind to the human VE-cadherin promoter (26). However, it was not known whether Snail could bind to the VE-cadherin promoter within the natural chromatin context of the cell.…”

Section: Tgf-␤1 Up-regulates Snail and Slug-tgf-␤1mentioning

confidence: 99%

“…human VE-cadherin promoter and suppress its promoter activity (26). In HTR-8/SVneo cells, treatment with TGF-␤1 up-regulated Snail and Slug mRNA levels in time-and dose-dependent manners (Fig.…”

Section: Tgf-␤1 Up-regulates Snail and Slug-tgf-␤1mentioning

confidence: 99%

See 3 more Smart Citations

Transforming Growth Factor-β1 Inhibits Trophoblast Cell Invasion by Inducing Snail-mediated Down-regulation of Vascular Endothelial-cadherin Protein

Cheng

Chang

2013

Journal of Biological Chemistry

104

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Background: Transforming growth factor (TGF)-␤1 treatment decreases human trophoblast invasion. Results: Smad-dependent up-regulation of Snail mediates TGF-␤1-induced down-regulation of VE-cadherin. Conclusion: TGF-␤1 decreases human trophoblast invasion by down-regulating VE-cadherin. Significance: Our results provide important insights into the molecular mechanisms mediating TGF-␤1-induced down-regulation of VE-cadherin and decreased cell invasion in human trophoblast cells.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Tgf-␤1 Up-regulates Snail and Slug-tgf-␤1mentioning

confidence: 99%

Section: Tgf-␤1 Up-regulates Snail and Slug-tgf-␤1mentioning

confidence: 99%

See 2 more Smart Citations

Transforming Growth Factor-β1 Inhibits Trophoblast Cell Invasion by Inducing Snail-mediated Down-regulation of Vascular Endothelial-cadherin Protein

Cheng

Chang

2013

Journal of Biological Chemistry

104

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“…The fibronectin matrix assembly is SPARCdependent (164). The up-regulated Twist, Snail and Slug proteins (165,166) together in malignantly transformed human cells repress the vascular endothelial VE-cadherin promoter (166).…”

Section: Malignant Cell Fusionsmentioning

confidence: 99%

Horizontal gene transfers and cell fusions in microbiology, immunology and oncology (Review)

Sinkovics¹

2009

Int J Oncol

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Modulating sphingosine‐1‐phosphate receptors to improve chemotherapy efficacy against Ewing sarcoma

Marmonti

Savage

Zhang

et al. 2020

Intl Journal of Cancer

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Tumor vasculature is innately dysfunctional. Poorly functional tumor vessels inefficiently deliver chemotherapy to tumor cells; vessel hyper‐permeability promotes chemotherapy delivery primarily to a tumor's periphery. Here, we identify a method for enhancing chemotherapy efficacy in Ewing sarcoma (ES) in mice by modulating tumor vessel permeability. Vessel permeability is partially controlled by the G protein‐coupled Sphinosine‐1‐phosphate receptors 1 and 2 (S1PR1 and S1PR2) on endothelial cells. S1PR1 promotes endothelial cell junction integrity while S1PR2 destabilizes it. We hypothesize that an imbalance of S1PR1:S1PR2 is partially responsible for the dysfunctional vascular phenotype characteristic of ES and that by altering the balance in favor of S1PR1, ES vessel hyper‐permeability can be reversed. In our study, we demonstrate that pharmacologic activation of S1PR1 by SEW2871 or inhibition of S1PR2 by JTE‐013 caused more organized, mature and functional tumor vessels. Importantly, S1PR1 activation or S1PR2 inhibition improved antitumor efficacy. Our data suggests that pharmacologic targeting of S1PR1 and S1PR2 may be a useful adjuvant to standard chemotherapy for ES patients.

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Tumor-induced upregulation of Twist, Snail, and Slug represses the activity of the human VE-cadherin promoter

Cited by 65 publications

References 20 publications

Transforming Growth Factor-β1 Inhibits Trophoblast Cell Invasion by Inducing Snail-mediated Down-regulation of Vascular Endothelial-cadherin Protein

Transforming Growth Factor-β1 Inhibits Trophoblast Cell Invasion by Inducing Snail-mediated Down-regulation of Vascular Endothelial-cadherin Protein

Horizontal gene transfers and cell fusions in microbiology, immunology and oncology (Review)

Modulating sphingosine‐1‐phosphate receptors to improve chemotherapy efficacy against Ewing sarcoma

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