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

Cheng, Jung‐Chien; Chang, Hsun‐Ming

doi:10.1074/jbc.m113.488866

Cited by 105 publications

(82 citation statements)

References 51 publications

(61 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…4C). Prolonged treatment with TGF-␤ alone was sufficient for Snail up-regulation and the induction of EMT, but it could not increase the number of CD44 high /CD24 low cells or Twist expression even in combination with TNF-␣, which was consistent with an earlier observation that TGF-␤ treatment minimally affects Twist expression (31,32).…”

Section: Involvement Of Tgf-␤/tnf-␣ Signaling Pathways In Has2-supporting

confidence: 80%

Excessive Hyaluronan Production Promotes Acquisition of Cancer Stem Cell Signatures through the Coordinated Regulation of Twist and the Transforming Growth Factor β (TGF-β)-Snail Signaling Axis

Chanmee

Ontong

Mochizuki

et al. 2014

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Hyaluronan overproduction is implicated in breast cancer progression. Results: Hyaluronan overproduction expands cancer stem-like cells through the up-regulation of Snail and Twist expression. Conclusion: Hyaluronan overproduction allows plastic cancer cells to revert to stem cell states via Twist and the transforming growth factor ␤-Snail signaling axis. Significance: These findings will help to understand the unique hyaluronan-dependent mechanisms that govern cancer cell plasticity and cancer stem cell expansion.

show abstract

Section: Involvement Of Tgf-␤/tnf-␣ Signaling Pathways In Has2-supporting

confidence: 80%

Excessive Hyaluronan Production Promotes Acquisition of Cancer Stem Cell Signatures through the Coordinated Regulation of Twist and the Transforming Growth Factor β (TGF-β)-Snail Signaling Axis

Chanmee

Ontong

Mochizuki

et al. 2014

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…In vitro studies demonstrate that TGFb1 increases the expression of E-cadherin, 30 a feature of cells in the epithelial state. TGFb1 also acts through 2 key transcriptional regulators of EMT in trophoblast cells; SNAIL 25 and TWIST, 33 which are discussed in the next section.…”

Section: Inducers Of Emtmentioning

confidence: 99%

“…TGFb plays crucial roles in regulating trophoblast cell adhesion, proliferation, differentiation, migration and invasion at the maternal-fetal interface. [25][26][27][28][29][30] TGFb exists in 3 different isoforms, with TGFb1 and TGFb2 thought to be the most important at the maternal-fetal interface. EVTs within the placental bed express TGFb2, while extracellular TGFb1 and cytoplasmic TGFb2 are localized within the decidua.…”

Section: Inducers Of Emtmentioning

confidence: 99%

Epithelial-mesenchymal transition during extravillous trophoblast differentiation

Davies

Pollheimer

Yong

et al. 2016

Cell Adhesion & Migration

214

146

View full text Add to dashboard Cite

A successful pregnancy depends on the intricate and timely interactions of maternal and fetal cells. Placental extravillous cytotrophoblast invasion involves a cellular transition from an epithelial to mesenchymal phenotype. Villous cytotrophoblasts undergo a partial epithelial to mesenchymal transition (EMT) when differentiating into extravillous cytotrophoblasts and gain the capacity to migrate and invade. This review summarizes our current knowledge regarding known regulators of EMT in the human placenta, including the inducers of EMT, upstream transcription factors that control EMT and the downstream effectors, cell adhesion molecules and their differential expression and functions in pregnancy pathologies, preeclampsia (PE) and fetal growth restriction (FGR). The review also describes the research strategies that were used for the identification of the functional role of EMT targets in vitro. A better understanding of molecular pathways driven by placental EMT and further elucidation of signaling pathways underlying the developmental programs may offer novel strategies of targeted therapy for improving feto-placental growth in placental pathologies including PE and FGR.

show abstract

“…The results of our study also confirmed that the TGF-β1-stimulated phosphorylation of Smad2/Smad3 had an influence on the EndMT in HCAECs. Snail and Slug are critical EndMT inducers, which allow the acquisition of mesenchymal phenotype through the regulation of several proteins related to EndMT, such as regressing VE-cadherin and E-cadherin, which are essential for endothelial cell-to-cell adhesion [30]. In addition, the TGF-β1/Smad signaling pathway has been found to be associated with plaque formation and rupture [31].…”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein A1 Inhibits the TGF-β1-Induced Endothelial-to-Mesenchymal Transition of Human Coronary Artery Endothelial Cells

Feng

Zhang²,

Jackson³

et al. 2017

Cardiology

View full text Add to dashboard Cite

Objective: Transforming growth factor β1 (TGF-β1) is the major cytokine for stimulating endothelial cells (ECs) to transdifferentiate to mesenchymal cells (MCs) in the process known as endothelial-to-mesenchymal transition (EndMT). Recently, TGF-β1-induced EndMT has been implicated in the pathogenesis of atherosclerosis (AS). It has been identified that apolipoprotein A1 (ApoA-I) obstructs TGF-β1-induced endothelial dysfunction, providing a protective effect for ECs and also anti-AS activity. However, the exact role of ApoA-I in TGF-β1-induced EndMT is not clear. In this study, we aimed to investigate whether ApoA-I can modulate TGF-β1-induced EndMT in human coronary artery ECs (HCAECs). Methods and Results: The HCAECs were treated with TGF-β1 with or without ApoA-I. Morphological changes in HCAECs and the expression of EndMT-related markers were evaluated. HCAECs treated with TGF-β1 were found to transform to MC morphology, with inconspicuous expression of EC markers such as vascular endothelial cadherin and CD31, and conspicuous expression of fibroblast-specific protein 1 (FSP-1) and α-smooth muscle actin. The treatment of HCAECs with ApoA-I inhibited the TGF-β1-induced EndMT, and elevated expression of EC markers was observed but reduced expression of MC markers. Moreover, ApoA-I impeded the expression level of Slug and Snail, crucial transcriptional factors of EndMT, and it inhibited the TGF-β1-induced phosphorylation of Smad2 and Smad3 which affected the EC morphology. In addition, the knockdown of ABCA1 by RNA interference eliminated the inhibition effect of ApoA-I on TGF-β1-induced EndMT. Conclusions: Our findings revealed a novel mechanism for the ApoA-I protective effect on endothelium function via the inhibition of TGF-β1-induced EndMT. This might provide new insights for developing strategies for modulating AS and vascular remodeling.

show abstract

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

Cited by 105 publications

References 51 publications

Excessive Hyaluronan Production Promotes Acquisition of Cancer Stem Cell Signatures through the Coordinated Regulation of Twist and the Transforming Growth Factor β (TGF-β)-Snail Signaling Axis

Excessive Hyaluronan Production Promotes Acquisition of Cancer Stem Cell Signatures through the Coordinated Regulation of Twist and the Transforming Growth Factor β (TGF-β)-Snail Signaling Axis

Epithelial-mesenchymal transition during extravillous trophoblast differentiation

Apolipoprotein A1 Inhibits the TGF-β1-Induced Endothelial-to-Mesenchymal Transition of Human Coronary Artery Endothelial Cells

Contact Info

Product

Resources

About