The Experts below are selected from a list of 55059 Experts worldwide ranked by ideXlab platform
Alfonso Bellacosa - One of the best experts on this subject based on the ideXlab platform.
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Epithelial Mesenchymal Transition in development and cancer role of phosphatidylinositol 3 kinase akt pathways
Oncogene, 2005Co-Authors: Lionel Larue, Alfonso BellacosaAbstract:Epithelial–Mesenchymal Transition in development and cancer: role of phosphatidylinositol 3′ kinase/AKT pathways
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Epithelial Mesenchymal Transition in development and cancer role of phosphatidylinositol 3 kinase akt pathways
Oncogene, 2005Co-Authors: Lionel Larue, Alfonso BellacosaAbstract:Epithelial–Mesenchymal Transition in development and cancer: role of phosphatidylinositol 3′ kinase/AKT pathways
Lionel Larue - One of the best experts on this subject based on the ideXlab platform.
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Epithelial Mesenchymal Transition in development and cancer role of phosphatidylinositol 3 kinase akt pathways
Oncogene, 2005Co-Authors: Lionel Larue, Alfonso BellacosaAbstract:Epithelial–Mesenchymal Transition in development and cancer: role of phosphatidylinositol 3′ kinase/AKT pathways
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Epithelial Mesenchymal Transition in development and cancer role of phosphatidylinositol 3 kinase akt pathways
Oncogene, 2005Co-Authors: Lionel Larue, Alfonso BellacosaAbstract:Epithelial–Mesenchymal Transition in development and cancer: role of phosphatidylinositol 3′ kinase/AKT pathways
Rumela Chakrabarti - One of the best experts on this subject based on the ideXlab platform.
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elf5 inhibits the Epithelial Mesenchymal Transition in mammary gland development and breast cancer metastasis by transcriptionally repressing snail2
Nature Cell Biology, 2012Co-Authors: Qifeng Yang, Rumela Chakrabarti, Julie Hwang, Mario Andres Blanco, Martin Lukacisin, Roseanne Romano, Kirsten Smalley, Toni IbrahimAbstract:Kang and colleagues show that the transcription factor Elf5 controls the Epithelial–Mesenchymal Transition (EMT) during development and in metastasis, by repressing the expression of Snail2/Slug, a key EMT-inducing factor.
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elf5 inhibits the Epithelial Mesenchymal Transition in mammary gland development and breast cancer metastasis by transcriptionally repressing snail2
Nature Cell Biology, 2012Co-Authors: Rumela Chakrabarti, Julie Hwang, Mario Andres Blanco, Martin Lukacisin, Roseanne Romano, Kirsten Smalley, Yong Wei, Song Liu, Qifeng YangAbstract:Kang and colleagues show that the transcription factor Elf5 controls the Epithelial–Mesenchymal Transition (EMT) during development and in metastasis, by repressing the expression of Snail2/Slug, a key EMT-inducing factor.
Qifeng Yang - One of the best experts on this subject based on the ideXlab platform.
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mdc1 promotes ovarian cancer metastasis by inducing Epithelial Mesenchymal Transition
Tumor Biology, 2015Co-Authors: Xiaolin Liu, Ruifen Dong, Zhijun Jiang, Yuyan Wei, Linxuan Wei, Hengzi Sun, Ning Yang, Qifeng Yang, Zhaojian Liu, Beihua KongAbstract:Ovarian cancer is a highly invasive cancer with poor prognosis. Previous studies have revealed lots of connections between the invasiveness and Epithelial-Mesenchymal Transition (EMT), which is common during the progression of ovarian cancer. MDC1, a mediator of DNA damage checkpoint, has recently been implicated as a potential oncogene. Here, in this article, we studied the role of MDC1 in ovarian cancer metastasis. First, in tissue samples, we found that high expression level of MDC1 was correlated with poor prognosis. Furthermore, MDC1 overexpression in ovarian cancer cells significantly increased migration and invasion. In contrast, silencing MDC1 reversed these processes. Consistently, nude mice xenograft confirmed that silencing MDC1 suppressed tumor metastasis in vivo. We further demonstrated that MDC1 induced EMT through modulation EMT markers such as E-cadherin, N-cadherin, and vimentin. Taken together, our findings suggest that MDC1 promotes ovarian cancer metastasis through the induction of EMT.
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elf5 inhibits the Epithelial Mesenchymal Transition in mammary gland development and breast cancer metastasis by transcriptionally repressing snail2
Nature Cell Biology, 2012Co-Authors: Qifeng Yang, Rumela Chakrabarti, Julie Hwang, Mario Andres Blanco, Martin Lukacisin, Roseanne Romano, Kirsten Smalley, Toni IbrahimAbstract:Kang and colleagues show that the transcription factor Elf5 controls the Epithelial–Mesenchymal Transition (EMT) during development and in metastasis, by repressing the expression of Snail2/Slug, a key EMT-inducing factor.
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elf5 inhibits the Epithelial Mesenchymal Transition in mammary gland development and breast cancer metastasis by transcriptionally repressing snail2
Nature Cell Biology, 2012Co-Authors: Rumela Chakrabarti, Julie Hwang, Mario Andres Blanco, Martin Lukacisin, Roseanne Romano, Kirsten Smalley, Yong Wei, Song Liu, Qifeng YangAbstract:Kang and colleagues show that the transcription factor Elf5 controls the Epithelial–Mesenchymal Transition (EMT) during development and in metastasis, by repressing the expression of Snail2/Slug, a key EMT-inducing factor.
Damian Medici - One of the best experts on this subject based on the ideXlab platform.
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signaling mechanisms of the Epithelial Mesenchymal Transition
Science Signaling, 2014Co-Authors: David M Gonzalez, Damian MediciAbstract:The Epithelial-Mesenchymal Transition (EMT) is an essential mechanism in embryonic development and tissue repair. EMT also contributes to the progression of disease, including organ fibrosis and cancer. EMT, as well as a similar Transition occurring in vascular endothelial cells called endothelial-Mesenchymal Transition (EndMT), results from the induction of transcription factors that alter gene expression to promote loss of cell-cell adhesion, leading to a shift in cytoskeletal dynamics and a change from Epithelial morphology and physiology to the Mesenchymal phenotype. Transcription program switching in EMT is induced by signaling pathways mediated by transforming growth factor β (TGF-β) and bone morphogenetic protein (BMP), Wnt-β-catenin, Notch, Hedgehog, and receptor tyrosine kinases. These pathways are activated by various dynamic stimuli from the local microenvironment, including growth factors and cytokines, hypoxia, and contact with the surrounding extracellular matrix (ECM). We discuss how these pathways crosstalk and respond to signals from the microenvironment to regulate the expression and function of EMT-inducing transcription factors in development, physiology, and disease. Understanding these mechanisms will enable the therapeutic control of EMT to promote tissue regeneration, treat fibrosis, and prevent cancer metastasis.