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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Book ChapterDOI
Heterogeneity and Plasticity of Breast Cancer Stem Cells.
TL;DR: This chapter will be mainly discussed the emerging knowledge regarding the contribution of BCSCs to tumour heterogeneity, their plasticity, and the role that this plasticity can play in the establishment of distant metastasis.
Journal ArticleDOI
miR-1236 regulates hypoxia-induced epithelial–mesenchymal transition and cell migration/invasion through repressing SENP1 and HDAC3
TL;DR: It is shown that miR-1236 plays a critical role in hypoxia-induced EMT and metastasis through repressing HDAC3 and SENP1 expression and present a regulatory network that involves many key players in hyp oxia- induced EMT.
Journal ArticleDOI
Overexpression of Nodal induces a metastatic phenotype in pancreatic cancer cells via the Smad2/3 pathway
Wanxing Duan,Rong Li,Jiguang Ma,Jianjun Lei,Qinhong Xu,Zhengdong Jiang,Ligang Nan,Xuqi Li,Zheng Wang,Xiongwei Huo,Liang Han,Zheng Wu,Erxi Wu,Qingyong Ma +13 more
TL;DR: The results suggest that Nodal overexpression induces a metastatic phenotype in pancreatic cancer cells, and that targeting NODal signaling may be a promising therapeutic strategy for pancreatic cancers.
Journal ArticleDOI
Tenascin-C induces migration and invasion through JNK/c-Jun signalling in pancreatic cancer.
Jun Cai,Shaoxia Du,Hui Wang,Beibei Xin,Juan Wang,Wenyuan Shen,Wei Wei,Zhongkui Guo,Xiaohong Shen +8 more
TL;DR: The data showed that TNC induced pancreatic cancer cells to generate an EMT phenotype and acquire motility potential through the activation of JNK/c-Jun signalling, and regulated a number of metastasis-associated proteins, including the EMT markers, MMP9 and Paxillin.
Journal ArticleDOI
DDR2 upregulation confers ferroptosis susceptibility of recurrent breast tumors through the Hippo pathway.
Chao-Chieh Lin,Wen-Hsuan Yang,Yi-Tzu Lin,Xiaohu Tang,Po-Han Chen,Chien-Kuang Cornelia Ding,Dan Chen Qu,James V. Alvarez,Jen-Tsan Chi +8 more
TL;DR: In this paper, the authors showed that EMT regulators, TWIST and SNAIL, significantly induce DDR2 expression and sensitize ferroptosis in a DDR2-dependent manner.
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