Epithelial–mesenchymal plasticity in carcinoma metastasis
Jeff H. Tsai,Jing Yang +1 more
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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.read more
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β-catenin activation down-regulates cell-cell junction-related genes and induces epithelial-to-mesenchymal transition in colorectal cancers.
Won Kyu Kim,Won Kyu Kim,Yu-Jin Kwon,Mi Jang,Minhee Park,Ji-Yoon Kim,Suyeon Cho,Dong Geon Jang,Wook Bin Lee,Sang Hoon Jung,Hye Jin Choi,Byung Soh Min,Tae Il Kim,Sung Pil Hong,Young Ki Paik,Hoguen Kim +15 more
TL;DR: The findings suggest that β-catenin activation induces EMT progression by modifying cell-cell junctions, and thereby contributes to CRC aggressiveness.
Journal ArticleDOI
The low affinity neurotrophin receptor CD271 regulates phenotype switching in melanoma
Gaetana Restivo,Johanna Diener,Phil F. Cheng,Gregor Kiowski,Mario Bonalli,Thomas Biedermann,Ernst Reichmann,Mitchell P. Levesque,Reinhard Dummer,Lukas Sommer +9 more
TL;DR: In vivo models of human melanoma are used and it is shown that CD271 is a key regulator of phenotype switching and metastasis formation, and plays a dual role in this process by decreasing proliferation, while simultaneously promoting invasiveness.
Journal ArticleDOI
Tumour progression and metastasis
TL;DR: The strategies that develop tumour cells during tumour progression and the way in which the microenvironment influences the formation of metastasis are reviewed and it is suggested that the metastatic niche can be an ideal target for new treatments that make controlling metastasis possible.
Journal ArticleDOI
The biological and clinical importance of epithelial–mesenchymal transition in circulating tumor cells
TL;DR: The biological and clinical importance of EMT and/or MET in CTCs during the individual steps of tumor metastasis are focused on, summarizing the recent findings of the regulatory roles played in the generation, survival, and recolonization of C TCs and discussing the EMT-targeting strategies developed for tumor diagnosis as well as their potential for management of metastatic malignant diseases.
Journal ArticleDOI
Acetylation of KLF5 maintains EMT and tumorigenicity to cause chemoresistant bone metastasis in prostate cancer.
Baotong Zhang,Yixiang Li,Qiao Wu,Lin Xie,Lin Xie,Benjamin G. Barwick,Changying Fu,Changying Fu,Xin Li,Daqing Wu,Siyuan Xia,Jing Chen,Weiping Qian,Lily Yang,Adeboye O. Osunkoya,Lawrence H. Boise,Paula M. Vertino,Yichao Zhao,Menglin Li,Hsiao Rong Chen,Jeanne Kowalski,Omer Kucuk,Wei Zhou,Jin-Tang Dong,Jin-Tang Dong +24 more
TL;DR: In this paper, the authors show that bone derived TGF-β induces the acetylation of transcription factor KLF5 (Ac-KLF5) in prostate cancer, which leads to osteoclastogenesis and bone metastatic lesions.
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