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Open AccessJournal ArticleDOI

Epithelial–mesenchymal plasticity in carcinoma metastasis

Jeff H. Tsai, +1 more
- 15 Oct 2013 - 
- Vol. 27, Iss: 20, pp 2192-2206
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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Citations
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Journal ArticleDOI

Short-term stimulation with histone deacetylase inhibitor trichostatin a induces epithelial-mesenchymal transition in nasopharyngeal carcinoma cells without increasing cell invasion ability.

TL;DR: It is indicated that short-term stimulation of TSA effectively inhibits cell proliferation and induce EMT-like changes in NPC cells but not increase its invasion ability.
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Preparation and Evaluation of Liposomes Co-Loaded with Doxorubicin, Phospholipase D Inhibitor 5-Fluoro-2-Indolyl Deschlorohalopemide (FIPI) and D-Alpha Tocopheryl Acid Succinate (α-TOS) for Anti-Metastasis

TL;DR: In vivo anti-metastasis study showed that DFT-Lip prevented the initiation and the progression of metastasis of high metastatic breast cancer, suggesting that the liposomes containing DOX, FIPI, and α-TOS might be a promising strategy for metastatic tumor therapy in clinics.
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Bovine lactoferrin reverses programming of epithelial-to-mesenchymal transition to mesenchymal-to-epithelial transition in oral squamous cell carcinoma

TL;DR: It is found that bLF changed the spindle-like mesenchymal cells to cuboidal-like epithelial cells and enhanced the affinity of membrane-bound E-cadherin in HOC313 cells, which is the first report indicating that b LF inhibited EMT and induced MET in OSCC.
Journal ArticleDOI

Yeast-derived recombinant avenanthramides inhibit proliferation, migration and epithelial mesenchymal transition of colon cancer cells

TL;DR: YAvns resulted more effective than natural compounds in inhibiting cancer cell migration and reverting major molecular features of the EMT process, including the down-regulation of E-cadherin mRNA and protein levels.
Journal ArticleDOI

Mesenchymal stem cells induce epithelial mesenchymal transition in melanoma by paracrine secretion of transforming growth factor-β.

TL;DR: This study shows that MSC induces EMT in melanoma cells in a paracrine manner, which might be mediated by the TGF-&bgr;/Snail signaling pathway, and caution should be exercised when considering MSCs-based therapy in melan cancer and also in other cancers.
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