ArticlePloS one2010
Retinoic acid mediates regulation of network formation by COUP-TFII and VE-cadherin expression by TGFbeta receptor kinase in breast cancer cells.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Cellular and micro-environmental responses influencing the antitumor activity of all-trans retinoic acid in breast cancer.Cell communication and signaling : CCS · 2024Review
- Effects of Functional and Nutraceutical Foods in the Context of the Mediterranean Diet in Patients Diagnosed with Breast Cancer.Antioxidants (Basel, Switzerland) · 2023Review
- Nutraceuticals in the Mediterranean Diet: Potential Avenues for Breast Cancer Treatment.Nutrients · 2021Review
- IL-1β Promotes Vasculogenic Mimicry of Breast Cancer Cells Through p38/MAPK and PI3K/Akt Signaling Pathways.Frontiers in oncology · 2021Article
- p38 MAPK signaling mediates retinoic acid-induced CD103 expression in human dendritic cells.Immunology · 2020Article
- COUP-TFII in Health and Disease.Cells · 2019Review
- miR-27b inhibits gastric cancer metastasis by targeting NR2F2.Protein & cell · 2017Article
- Transcriptional Factors Mediating Retinoic Acid Signals in the Control of Energy Metabolism.International journal of molecular sciences · 2015Review
- COUP-TFII regulates metastasis of colorectal adenocarcinoma cells by modulating Snail1.British journal of cancer · 2014Article
- Expression and functional pathway analysis of nuclear receptor NR2F2 in ovarian cancer.The Journal of clinical endocrinology and metabolism · 2013Article
- Multiple roles of COUP-TFII in cancer initiation and progression.Journal of molecular endocrinology · 2012Review
- Maternal smoking and the retinoid pathway in the developing lung.Respiratory research · 2012Article
- Mesodermal retinoic acid signaling regulates endothelial cell coalescence in caudal pharyngeal arch artery vasculogenesis.Developmental biology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Tumor development, growth, and metastasis depend on the provision of an adequate vascular supply. This can be due to regulated angiogenesis, recruitment of circulating endothelial progenitors, and/or vascular transdifferentiation. Our previous studies showed that retinoic acid (RA) treatment converts a subset of breast cancer cells into cells with significant endothelial genotypic and phenotypic elements including marked induction of VE-cadherin, which was responsible for some but not all morphological changes. The present study demonstrates that of the endothelial-related genes induced by RA treatment, only a few were affected by knockdown of VE-cadherin, ruling it out as a regulator of the RA-induced endothelial genotypic switch. In contrast, knockdown of the RA-induced gene COUP-TFII prevented the formation of networks in Matrigel but had no effect on VE-cadherin induction or cell fusion. Two pan-kinase inhibitors markedly blocked RA-induced VE-cadherin expression and cell fusion. However, RA treatment resulted in a marked and broad reduction in tyrosine kinase activity. Several genes in the TGFbeta signaling pathway were induced by RA, and specific inhibition of the TGFbeta type I receptor blocked both RA-induced VE-cadherin expression and cell fusion. Together these data indicate a role for the TGFbeta pathway and COUP-TFII in mediating the endothelial transdifferentiating properties of RA.
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