Epithelial-mesenchymal transition (EMT), a cellular phenotypic change from epithelial to mesenchymal-like features, is related to the resistance and metastasis of cancer stem cells (CSCs). Several signal transduction mechanisms induce EMT, which causes the gene expression alteration to induce the acquisition of resistance and metastasis in cancer. EMT is characterized with high gene expression of cadherin 2 (N-cadherin) and vimentin, and sparse cell-cell junction. The cells with EMT-phenotype have migration, metastasis and drug-resistance capacity, which are main characteristics of CSCs. It seems that the main population of CSCs exhibits EMT phenotype, whereas some populations consist of phenotypes other than EMT. In this chapter, EMT mechanism, phenotypic features of EMT and CSCs, signal transduction in EMT and CSCs, differences between EMT and CSCs, and the role of EMT in CSCs are described.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/978-3-031-12974-2_1 | DOI Listing |
Cells
December 2024
Translational Medicine, School of Science, Engineering and Environment (SEE), University of Salford, Greater Manchester, Salford M5 4WT, UK.
Cancer stem cells (CSCs) account for 0.01 to 2% of the total tumor mass; however, they play a key role in tumor progression, metastasis and resistance to current cancer therapies. The generation and maintenance of CSCs are usually linked to the epithelial-mesenchymal transition (EMT), a dynamic process involved in reprogramming cancer cells towards a more aggressive and motile phenotype with increased stemness potential.
View Article and Find Full Text PDFJ Biochem
January 2025
Laboratory of Anticancer Strategies, Advanced Research Initiative, Institute of Science Tokyo, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan.
Cell Biol Int
December 2024
Cellular and Molecular Oncobiology Program, Brazilian National Cancer Institute (INCA), Rio de Janeiro, Brazil.
The high plasticity of cells undergoing epithelial-mesenchymal transition (EMT) promotes increased tumor heterogeneity, and its interaction with tumor-associated stromal cells appears to contribute to developing a stemness phenotype. Cells with these characteristics exhibit increased resistance to chemotherapy and radiotherapy, leading to disease relapse and metastasis. Here, we discuss the activation of the Wnt/β-catenin pathway in promoting EMT and stemness within the context of cellular resistance to these therapies.
View Article and Find Full Text PDFCell Biol Toxicol
December 2024
Department of General Surgery, First Medical Center of Chinese, PLA General Hospital, Haidian District, No.28 Fuxing Road, Beijing, 100853, China.
Accumulating evidences have indicated that cancer stem cells (CSCs) can initiate tumor progression and cause recurrence after therapy. However, specific markers of gastric CSCs (GCSCs) from different origins have not been comprehensively revealed. Here, we further detected whether cell populations labelled with CD44 and Lgr5, well-recognized stem markers for gastric cancer (GC), can better emphasize cancer initiation, therapeutic resistance and recurrence.
View Article and Find Full Text PDFCancer Cell Int
December 2024
Laboratory for Personalized Medicine, Division of Molecular Medicine, Rudjer Boskovic Institute, Bijenicka 54, Zagreb, 10000, Croatia.
Background: The development of resistance to therapy is characteristic of head and neck squamous cell carcinoma (HNSCC), the 6th most common cancer, and is often attributed to cancer stem cells (CSCs). By proteomic approach, we determined that UFMylation plays an important role in HNSCC CSCs. Because of the necessity for innovative therapeutic strategies, we explore here the therapy targeting CSCs based on mithramycin and its inhibitory effect on Sp1 transcription factor, UFMylation, and CSCs survival and stemness.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!