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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Association of DCBLD2 upregulation with tumor progression and poor survival in colorectal cancer
Jie He,Hongli Huang,Yanlei Du,Dong Peng,Youlian Zhou,Yuyuan Li,Hong Wang,Yongjian Zhou,Yuqiang Nie +8 more
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WAVE3 promotes epithelial–mesenchymal transition of gastric cancer through upregulation of Snail
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Exposure to desflurane anesthesia confers colorectal cancer cells metastatic capacity through deregulation of miR-34a/LOXL3.
TL;DR: Clinical miR-34a mimic or inhibitor targeting LOXL3 might have a potential protective role when patients with CRC anesthetized by desflurane and show more lymph node metastasis, as well as poor survival.
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Downregulated vimentin and upregulated E-cadherin in T1 stage non-small-cell lung cancer: does it suggest a mesenchymal-epithelial transition?
TL;DR: The study results suggest that a mesenchymal-epithelial transition may take place in the early-stage of tumor development, and that EMT occurs when the tumor develops into a certain stage.
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Acetate promotes SNAI1 expression by ACSS2-mediated histone acetylation under glucose limitation in renal cell carcinoma cell.
TL;DR: A novel inducer, acetate, is identified, which can promote SNAI1 expression by ACSS2-mediated histone acetylation in partly, which has important implication in treatment of metastatic cancers.
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