Choose your destiny: Make a cell fate decision with COUP-TFII

Wu, San‐Pin; Yu, Cheng-Tai; Tsai, Sophia Y.; Tsai, Ming‐Jer

doi:10.1016/j.jsbmb.2015.11.011

Cited by 23 publications

(26 citation statements)

References 96 publications

(121 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Several studies have reported that NR2F2 is a critical nuclear receptor in cardiovascular development [9][10][11][12], but we demonstrate that this nuclear receptor has a different molecular function in breast cancer. In this paper, we investigated the gene expression level of NR2F2 in patients with different breast cancer subtypes.…”

Section: Introductionmentioning

confidence: 48%

NR2F2 Orphan Nuclear Receptor is Involved in Estrogen Receptor Alpha-Mediated Transcriptional Regulation in Luminal A Breast Cancer Cells

Erdős

Bálint

2020

IJMS

View full text Add to dashboard Cite

Nuclear Receptor Subfamily 2 Group F Member 2 (NR2F2) is a member of the steroid/thyroid hormone receptor superfamily with a crucial role in organogenesis, angiogenesis, cardiovascular development and tumorigenesis. However, there is limited knowledge about the cistrome and transcriptome of NR2F2 in breast cancer. In this study, we mapped the regulatory mechanism by NR2F2 using functional genomic methods. To investigate the clinical significance of NR2F2 in breast cancer, The Cancer Genome Atlas (TCGA) data were used. These results show that a high NR2F2 is associated with better survival of a specific subset of patients, namely those with luminal A breast cancer. Therefore, genome-wide NR2F2 and estrogen receptor alpha (ERα) binding sites were mapped in luminal A breast cancer cells using chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-Seq), revealing that most NR2F2 overlap with ERα that are co-occupied by forkhead box A1 (FOXA1) and GATA binding protein 3 (GATA3) in active enhancer regions. NR2F2 overlaps with highly frequent ERα chromatin interactions, which are essential for the formation of ERα-bound super-enhancers. In the process of the transcriptome profiling of NR2F2-depleted breast cancer cells such differentially expressed genes have been identified that are involved in endocrine therapy resistance and are also ERα target genes. Overall, these findings demonstrate that the NR2F2 nuclear receptor has a key role in ERα-mediated transcription and it can offer a potential therapeutic target in patients with luminal A breast cancer.

show abstract

Section: Introductionmentioning

confidence: 48%

NR2F2 Orphan Nuclear Receptor is Involved in Estrogen Receptor Alpha-Mediated Transcriptional Regulation in Luminal A Breast Cancer Cells

Erdős

Bálint

2020

IJMS

View full text Add to dashboard Cite

show abstract

“…COUP-TFII is expressed by several cell types including endothelial cells (Wu et al, 2016). In the vascular system, COUP-TFII has been shown to regulate venous EC identity as well as lymphatic EC specification (You et al, 2005; Lin et al, 2010; Srinivasan et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Angiopoietin receptor Tie2 is required for vein specification and maintenance via regulating COUP-TFII

Chu

Shen

et al. 2016

eLife

View full text Add to dashboard Cite

Mechanisms underlying the vein development remain largely unknown. Tie2 signaling mediates endothelial cell (EC) survival and vascular maturation and its activating mutations are linked to venous malformations. Here we show that vein formation are disrupted in mouse skin and mesentery when Tie2 signals are diminished by targeted deletion of Tek either ubiquitously or specifically in embryonic ECs. Postnatal Tie2 attenuation resulted in the degeneration of newly formed veins followed by the formation of haemangioma-like vascular tufts in retina and venous tortuosity. Mechanistically, Tie2 insufficiency compromised venous EC identity, as indicated by a significant decrease of COUP-TFII protein level, a key regulator in venogenesis. Consistently, angiopoietin-1 stimulation increased COUP-TFII in cultured ECs, while Tie2 knockdown or blockade of Tie2 downstream PI3K/Akt pathway reduced COUP-TFII which could be reverted by the proteasome inhibition. Together, our results imply that Tie2 is essential for venous specification and maintenance via Akt mediated stabilization of COUP-TFII.DOI: http://dx.doi.org/10.7554/eLife.21032.001

show abstract

“…Chicken Ovalbumin Upstream Promoter-Transcription Factor II ( COUP-TFII , also known as Nr2f2 ) is an orphan member of the steroid/thyroid hormone receptor superfamily. Previous studies showed that COUP-TFII can function as a transcriptional repressor through direct binding to COUP-TFII response elements or a transcriptional activator by associating with specific transcriptional factors to regulate their target genes in diverse cellular contexts 17 , 18 . COUP-TFII is expressed abundantly during the early embryonic stage.…”

Section: Introductionmentioning

confidence: 99%

COUP-TFII is required for morphogenesis of the neural crest-derived tympanic ring

Hsu

Chen²,

You³

2017

Sci Rep

View full text Add to dashboard Cite

Chicken Ovalbumin Upstream Promoter-Transcription Factor II (COUP-TFII) plays pivotal roles in cell growth, cell differentiation, and cell fate determination. Although genome-wide studies have identified COUP-TFII binding on gene sets mainly involved in neural crest cell (NCC) development and craniofacial morphogenesis, the direct functional connection between COUP-TFII and NCCs in vivo has not been well characterized. In this study, we show that COUP-TFII is expressed in the subpopulation of NCCs and its derivatives, and targeted ablation of COUP-TFII in mouse NCCs results in markedly shortened and bifurcated tympanic rings, which in turn disturb the caudal direction of external acoustic meatus invagination. However, formation of the manubrium of the malleus (MM) in Wnt1-Cre/+;COUP-TFII flox/flox mice is not perturbed, suggesting that the rostral half of the tympanic ring is sufficient to support proper MM development. Interestingly, we found that loss of COUP-TFII up-regulates Sox9 in the tympanic ring primordium and affects the distribution of preosteoblasts before mesenchymal condensation. Together, our results demonstrate that COUP-TFII plays an essential role in regulating the patterning of the NCC-derived tympanic ring.

show abstract

Choose your destiny: Make a cell fate decision with COUP-TFII

Cited by 23 publications

References 96 publications

NR2F2 Orphan Nuclear Receptor is Involved in Estrogen Receptor Alpha-Mediated Transcriptional Regulation in Luminal A Breast Cancer Cells

NR2F2 Orphan Nuclear Receptor is Involved in Estrogen Receptor Alpha-Mediated Transcriptional Regulation in Luminal A Breast Cancer Cells

Angiopoietin receptor Tie2 is required for vein specification and maintenance via regulating COUP-TFII

COUP-TFII is required for morphogenesis of the neural crest-derived tympanic ring

Contact Info

Product

Resources

About