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The basics of epithelial-mesenchymal transition

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TLDR
Processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias and the identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes.
Abstract
The origins of the mesenchymal cells participating in tissue repair and pathological processes, notably tissue fibrosis, tumor invasiveness, and metastasis, are poorly understood. However, emerging evidence suggests that epithelial-mesenchymal transitions (EMTs) represent one important source of these cells. As we discuss here, processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias. The identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes and possible therapeutic interventions.

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Epithelial-mesenchymal transition in cervical carcinoma.

TL;DR: An up-to-date overview regarding the program of EMT in cervical cancer is provided and transcriptional factors such as Snail, Twist1, Twist2, and six1 homeoproteins are involved in the complicated regulation and cervical cancer metastasis.
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Combinatorial interventions inhibit TGFβ-driven epithelial-to-mesenchymal transition and support hybrid cellular phenotypes.

TL;DR: The results indicate that EMT is driven by an interconnected signaling network and many apparently successful single interventions may lead to steady states that are in-between epithelial and mesenchymal states, and suggest that combinatorial therapies are necessary to fully suppress invasive properties of tumor cells.
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Breast cancer stem cells: Features, key drivers and treatment options.

TL;DR: A large body of knowledge has been accumulated regarding the signaling cascades and proteins involved in maintaining stemness in breast cancer, and differences in the stem cell pool size and in mechanisms regulatingstemness in the different breast cancer subtypes have emerged.
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Regulation of cancer metastasis by microRNAs

TL;DR: This review will summarize the recent findings and characterization of miRNAs that are involved in the regulation of EMT, migration, invasion and metastasis of cancer cells, and discuss potential use of mi RNAs as diagnostic and prognostic biomarkers as well as therapeutic targets for cancer.
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Durotaxis by Human Cancer Cells

TL;DR: These durotaxis assays demonstrated that all cancer cell lines tested (two glioblastoma, metastatic breast cancer, and fibrosarcoma) migrated directionally in response to changes in extracellular stiffness, and inhibition of Arp2/3, an actin-nucleating protein necessary for lamellipodial protrusion, impaired durotactic migration.
References
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Journal ArticleDOI

The hallmarks of cancer.

TL;DR: This work has been supported by the Department of the Army and the National Institutes of Health, and the author acknowledges the support and encouragement of the National Cancer Institute.
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The Epithelial-Mesenchymal Transition Generates Cells with Properties of Stem Cells

TL;DR: It is reported that the induction of an EMT in immortalized human mammary epithelial cells (HMLEs) results in the acquisition of mesenchymal traits and in the expression of stem-cell markers, and it is shown that those cells have an increased ability to form mammospheres, a property associated with mammARY epithelial stem cells.
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Epithelial–mesenchymal transitions in tumour progression

TL;DR: Epithelial–mesenchymal transition provides a new basis for understanding the progression of carcinoma towards dedifferentiated and more malignant states.
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Mechanisms of TGF-β Signaling from Cell Membrane to the Nucleus

TL;DR: Current understanding on the mechanisms of TGF-β signaling from cell membrane to the nucleus is presented and the transcriptional regulation of target gene expression is reviewed.
Journal ArticleDOI

Complex networks orchestrate epithelial–mesenchymal transitions

TL;DR: Understanding how mesenchymal cells arise from an epithelial default status will also have a strong impact in unravelling the mechanisms that control fibrosis and cancer progression.
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