G protein‐coupled estrogen receptor 1 inhibits the epithelial‐mesenchymal transition of goat mammary epithelial cells via NF‐κB signaling pathway

2021 ◽  
Author(s):  
Ying Zhao ◽  
Zhenshan Yang ◽  
Yuyang Miao ◽  
Mingzhen Fan ◽  
Xiaoe Zhao ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Epithelial Cells ◽  
G Protein ◽  
Epithelial Mesenchymal Transition ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Mesenchymal Transition ◽  
G Protein Coupled ◽  
Estrogen Receptor 1 ◽  
Goat Mammary Epithelial Cells

Extracellular vesicles from women with breast cancer promote an epithelial-mesenchymal transition-like process in mammary epithelial cells MCF10A

Tumor Biology ◽  
2015 ◽  
Vol 36 (12) ◽  
pp. 9649-9659 ◽  
Author(s):  
Octavio Galindo-Hernandez ◽  
Cristina Gonzales-Vazquez ◽  
Pedro Cortes-Reynosa ◽  
Emmanuel Reyes-Uribe ◽  
Sonia Chavez-Ocaña ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Extracellular Vesicles ◽  
Epithelial Mesenchymal Transition ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Mesenchymal Transition

Overexpression of c-myc induces epithelial mesenchymal transition in mammary epithelial cells

2010 ◽  
Vol 293 (2) ◽  
pp. 230-239 ◽  
Author(s):  
Kyoung Bin Cho ◽  
Min Kyong Cho ◽  
Won Young Lee ◽  
Keon Wook Kang
Keyword(s):  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Mesenchymal Transition

scholarly journals Upregulated-flotillins and sphingosine kinase 2 derail vesicular trafic to stabilize AXL and promote epithelial-mesenchymal transition

2020 ◽  
Author(s):  
Mallory Genest ◽  
Franck Comunale ◽  
Damien Planchon ◽  
Pauline Govindin ◽  
Sophie Vacher ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Epithelial Mesenchymal Transition ◽  
Mammary Epithelial Cells ◽  
Sphingosine Kinase ◽  
Vesicular Trafficking ◽  
Mammary Epithelial ◽  
Lipid Kinase ◽  
Mesenchymal Transition ◽  
Sphingosine Kinase 2

AbstractAltered endocytosis and vesicular trafficking are major players during tumorigenesis. Flotillin overexpression, a feature observed in many invasive tumors, and identified as a marker of poor prognosis, induces a deregulated endocytic and trafficking pathway called Upregulated Flotillin-Induced Trafficking (UFIT). Here, we found that, in non tumoral mammary epithelial cells, induction of the UFIT pathway promotes epithelial-to-mesenchymal transition (EMT) and accelerates the endocytosis of several transmembrane receptors, including AXL, in flotillin-positive late endosomes. AXL overexpression, frequently observed in cancer cells, is linked to EMT and metastasis formation. In flotillin-overexpressing non-tumoral mammary epithelial cells and in invasive breast carcinoma cells, we found that the UFIT-mediated AXL endocytosis allows its stabilization and depends on sphingosine-kinase 2, a lipid kinase recruited in flotillin-rich plasma membrane-domains and endosomes.Thus, the deregulation of vesicular trafficking following flotillin upregulation, and through sphingosine kinase 2, emerges as a new mechanism of AXL overexpression and EMT-inducing signaling pathway activation.

Activation of G Protein-coupled Receptor 30 Promotes Proliferation of Goat Mammary Epithelial Cells via MEK/Erk&PI3K/Akt Signaling Pathway

2020 ◽  
Author(s):  
Ying Zhao ◽  
Haokun Liu ◽  
Mingzhen Fan ◽  
Yuyang Miao ◽  
Xiaoe Zhao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Epithelial Cells ◽  
Cyclin D1 ◽  
Mammary Epithelial Cells ◽  
Cyclin B1 ◽  
Akt Signaling ◽  
Mammary Epithelial ◽  
M Phase ◽  
G Protein Coupled ◽  
Goat Mammary Epithelial Cells

Abstract BackgroundGoat is an important dairy animal. During lactation, maintaining a high proliferative activity in goat mammary epithelial cells (GMECs) is significant to improve the yield and composition of goat milk. Estrogen is an essential hormone in epithelial cell proliferation and ductal morphogenesis of mammary gland. G protein-coupled receptor 30 (GPR30) is a novel membrane receptor of estrogen. However, the relationship between estrogen/GPR30 signaling and proliferation of goat mammary epithelial cells has not been reported. And the molecular mechanisms underlying the proliferative effect of estrogen via GPR30 on GMECs remain unclear.ResultsTo investigate the effect of estrogen/GPR30 signaling on GMECs proliferation, goat mammary epithelial cells, which expressed cytokeratin 18 and β-casein, were isolated and identified, defining their mammary alveolar epithelium origination. Estrogen and GPR30 agonist G1 obviously promoted the proliferation of GEMCs, in contrast, GPR30 antagonist G15 partly abolished estrogen-induced cell proliferation. Remarkably, the stimulatory effect of estrogen and G1 on GMECs growth was suppressed by GPR30 knockdown detected by cell counting assay, CCK-8 assay, and BrdU assay, suggesting that estrogen/GPR30 signaling was involved in GMECs proliferation. Additionally, G15 decreased cyclin D1, cyclin B1, CDK1, and p-CDK1 expression, resulting in cell cycle arrest in the G2/M phase via a down-regulated phosphorylation of Erk1/2 and Akt compared with estrogen alone. What’s more, knock-down GPR30 led to an accumulation in the G2/M phase and inhibition of cyclin D1, cyclin B1, CDK1, and p-CDK1 expression via a down-regulation of phosphorylated Erk1/2 and Akt despite the presence of estrogen and G1. Furthermore, MEK inhibitor and PI3K inhibitor decreased the expression of cyclin D1, cyclin B1, CDK1, and p-CDK1, and repressed estrogen-induced and G1-driven promotion of cell growth. It indicated that estrogen/GPR30 signaling played an important role in GMECs proliferation by affecting cell cycle progression via MEK/Erk&PI3K/Akt signaling pathway.ConclusionThis study may provide a new insight into the effect of estrogen/GPR30 signaling on the regulatory action of goat mammary gland development.

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