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 Regulation of Epithelial-Mesenchymal Transition in Breast Cancer Cells by Cell Contact and Adhesion

2015 ◽  
Vol 14s3 ◽  
pp. CIN.S18965 ◽  
Author(s):  
Magdalena A. Cichon ◽  
Celeste M. Nelson ◽  
Derek C. Radisky
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Rna Splicing ◽  
Epithelial Mesenchymal Transition ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Cell Contact ◽  
Mesenchymal Transition ◽  
Matrix Metalloproteinase 3 ◽  
Expression Of Genes

Epithelial-mesenchymal transition (EMT) is a physiological program that is activated during cancer cell invasion and metastasis. We show here that EMT-related processes are linked to a broad and conserved program of transcriptional alterations that are influenced by cell contact and adhesion. Using cultured human breast cancer and mouse mammary epithelial cells, we find that reduced cell density, conditions under which cell contact is reduced, leads to reduced expression of genes associated with mammary epithelial cell differentiation and increased expression of genes associated with breast cancer. We further find that treatment of cells with matrix metalloproteinase-3 (MMP-3), an inducer of EMT, interrupts a defined subset of cell contact-regulated genes, including genes encoding a variety of RNA splicing proteins known to regulate the expression of Rac1b, an activated splice isoform of Rac1 known to be a key mediator of MMP-3-induced EMT in breast, lung, and pancreas. These results provide new insights into how MMPs act in cancer progression and how loss of cell-cell interactions is a key step in the earliest stages of cancer development.

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.

scholarly journals The glucocorticoid receptor interferes with progesterone receptor-dependent genomic regulation in breast cancer cells

2019 ◽  
Vol 47 (20) ◽  
pp. 10645-10661 ◽  
Author(s):  
Maria F Ogara ◽  
Santiago A Rodríguez-Seguí ◽  
Melisa Marini ◽  
Ana Silvina Nacht ◽  
Martin Stortz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Mammary Epithelial Cells ◽  
Tumor Therapy ◽  
Progesterone Receptors ◽  
Cancer Cell Line ◽  
Mammary Epithelial ◽  
Chromatin Remodelers ◽  
Mesenchymal Transition ◽  
In Cells

Abstract The glucocorticoid and progesterone receptors (GR and PR) are closely related members of the steroid receptor family. Despite sharing similar structural and functional characteristics; the cognate hormones display very distinct physiological responses. In mammary epithelial cells, PR activation is associated with the incidence and progression of breast cancer, whereas the GR is related to growth suppression and differentiation. Despite their pharmacological relevance, only a few studies have compared GR and PR activities in the same system. Using a PR+/GR+ breast cancer cell line, here we report that either glucocorticoid-free or dexamethasone (DEX)-activated GR inhibits progestin-dependent gene expression associated to epithelial-mesenchymal-transition and cell proliferation. When both receptors are activated with their cognate hormones, PR and GR can form part of the same complex according to co-immunoprecipitation, quantitative microscopy and sequential ChIP experiments. Moreover, genome-wide studies in cells treated with either DEX or R5020, revealed the presence of several regions co-bound by both receptors. Surprisingly, GR also binds novel genomic sites in cells treated with R5020 alone. This progestin-induced GR binding was enriched in REL DNA motifs and located close to genes coding for chromatin remodelers. Understanding GR behavior in the context of progestin-dependent breast cancer could provide new targets for tumor therapy.

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