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Epithelial–mesenchymal plasticity in carcinoma metastasis

Jeff H. Tsai, +1 more
- 15 Oct 2013 - 
- Vol. 27, Iss: 20, pp 2192-2206
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TLDR
The functional requirement of EMT and/or MET during the individual steps of tumor metastasis is reviewed and the potential of targeting this program when treating metastatic diseases is discussed.
Abstract
Tumor metastasis is a multistep process by which tumor cells disseminate from their primary site and form secondary tumors at a distant site. Metastasis occurs through a series of steps: local invasion, intravasation, transport, extravasation, and colonization. A developmental program termed epithelial-mesenchymal transition (EMT) has been shown to play a critical role in promoting metastasis in epithelium-derived carcinoma. Recent experimental and clinical studies have improved our knowledge of this dynamic program and implicated EMT and its reverse program, mesenchymal-epithelial transition (MET), in the metastatic process. Here, we review the functional requirement of EMT and/or MET during the individual steps of tumor metastasis and discuss the potential of targeting this program when treating metastatic diseases.

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The long non-coding RNA LIMT inhibits metastasis of hepatocellular carcinoma and is suppressed by EGF signaling

TL;DR: In this paper , the effects of long non-coding RNA LIMT on tumor growth and metastasis were assessed by in vitro experiments, including colony formation and transwell assays, and in vivo in nude mouse models.

The Role of p120catenin in the Initiation and Dissemination of Pancreatic Cancer

Basil S Bakir
TL;DR: It is demonstrated, using multiple complementary mouse models, that liver and lung metastatic organotropism in pancreatic cancer is dependent on p120catenin (p120ctn)-mediated epithelial identity and RNA-seq demonstrates differential induction of pathways associated with metastasis and epithelial-to-mesenchymal transition in p 120ctn-deficient versus p120ctN-wild-type cells.
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MicroRNA-204 attenuates the migration and invasion of pancreatic cancer cells by targeting ZEB1/EMT axis.

TL;DR: The findings demonstrated the tumor suppressive role of miR-204 in PC through the ZEB1/EMT axis, therefore providing a novel therapeutic target for human PC.

Targeting the Epithelial-to-Mesenchymal Transition: The Case for Differentiation-Based Therapy

TL;DR: The epithelial-to-mesenchymal transition (EMT) as mentioned in this paper is a well-known cell-biological program that can confer an ability to disseminate, the ability to become stem-like tumor-initiating cells, and an elevated resistance to therapy.
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TL;DR: 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.
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