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
Citations
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The PIAS3-Smurf2 sumoylation pathway suppresses breast cancer organoid invasiveness.
TL;DR: The E3 ubiquitin ligase Smurf2 acts in a sumoylation-dependent manner to suppress the invasive behavior of MDA-MB-231 human breast cancer cell-derived organoids and the SUMO E3 ligase PIAS3 inhibits the invasive growth of breast cancer-cell derived organoids.
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Programming of macrophages by UV-irradiated apoptotic cancer cells inhibits cancer progression and lung metastasis
TL;DR: The injection of apoptotic lung cancer cells may offer a new strategy for the prevention of lung metastasis in syngeneic immunocompetent mice with enhanced PPARγ/PTEN signaling both in tumor-associated macrophages and in tumor cells.
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Recent Advances in Cancer Plasticity: Cellular Mechanisms, Surveillance Strategies, and Therapeutic Optimization.
TL;DR: An overview of recent advancements in understanding the mechanisms regulating cell plasticity and current strategies for their monitoring and therapy management is provided.
Journal ArticleDOI
Gambogenic acid induces ferroptosis in melanoma cells undergoing epithelial-to-mesenchymal transition.
TL;DR: It is suggested that GNA induces ferroptosis in TGF-β1-stimulated melanoma cells via the p53/SLC7A11/GPX4 signaling pathway and upregulated the expression of p53, solute carrier family 7 member 11 and glutathione peroxidase 4 in the model cells, contributing to the mechanisms underlying GNA-induced ferroPTosis.
Book ChapterDOI
Adipocytes in the Tumour Microenvironment.
TL;DR: This chapter discusses the diverse aspects of adipocytes and adipocyte-derived factors that affect the TME as well as tumour progression and metastasis, focus primarily on breast cancer but discuss what is known in other cancer types when relevant.
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