Generation of Breast Cancer Stem Cells through Epithelial-Mesenchymal Transition

By A. Morel, M. Lièvre, Clémence Thomas, George W. Hinkal, S. Ansieau, A. Puisieux. PLoS ONE, 2008

1,644 citations recorded by the source corpus.

Recently, two novel concepts have emerged in cancer biology: the role of so-called “cancer stem cells” in tumor initiation, and the involvement of an epithelial-mesenchymal transition (EMT) in the metastatic dissemination of epithelial cancer cells. Using a mammary tumor progression model, we show that cells possessing both stem and tumorigenic characteristics of “cancer stem cells” can be derived from human mammary epithelial cells following the activation of the Ras-MAPK pathway. The acquisition of these stem and tumorigenic characters is driven by EMT induction.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/fcdd6af594c5cf4936eaec866f78485f64bdafad

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Citations in the corpus

Dynamic EMT: a multi‐tool for tumor progression (2021, neutral): “Overexpression of SNAI1 , TWIST1 , and ZEB1 in breast cancer is sufficient to increase the CD44 + /CD24 lo stem cell pool, resulting in increased sphere forming capacity in vitro , as well as elevated tumorigenicity and metastasis in vivo (Mani et al , 2008; Morel et al , 2008).”
Epithelial–mesenchymal plasticity in carcinoma metastasis (2013, methodology): “Studies by the Weinberg group (Mani et al. 2008) and the Puisieux group (Morel et al. 2008) showed that activation of EMT by TGF-b, Snail1, Twist1, and Zeb1 in normal human mammary epithelial cells can promote a CSClike phenotype with tumor-initiating properties.”
Paracrine and autocrine signals induce and maintain mesenchymal and stem cell states in the breast (2011, background): “In addition, certain epithelial cells that pass through an EMT acquire the self-renewing trait associated with normal tissue (SCs) and cancer stem cells (CSCs) (Mani et al., 2008; Morel et al., 2008).”
The ZEB/miR‐200 feedback loop—a motor of cellular plasticity in development and cancer? (2010, background): “Such a link was described at the molecular level, showing that the EMt acti vator twist can induce stem-cell properties in mammary epithelial cells (Mani et al, 2008; Morel et al, 2008).”
Poised chromatin at the ZEB1 promoter enables cell plasticity and enhances tumorigenicity (2013, neutral): “consistent with the idea that the epithelial-mesenchymal transition generates cells with CSClike activity (Mani et al., 2008; Morel et al., 2008).”
Epithelial-mesenchymal plasticity in cancer progression and metastasis (2019, background): “Experimental overexpression of SNAI1, SNAI2 or TWIST in immortalized or transformed human mammary epithelial cells leads to a stem cell phenotype with increased sphere-forming ability and expression of stem cell markers, whereas their inhibition blocks mammary gland reconstitution and tumor initiati”
Epithelial-Mesenchymal Plasticity: A central regulator of cancer progression (2015, background): “Moreover, CSCs have been found to exhibit a heightened resistance to a variety of existing treatments, including radio-and chemotherapy in various carcinoma types (Creighton et al., 2009; Singh and Settleman, 2010).”
Epithelial Plasticity: A Common Theme in Embryonic and Cancer Cells (2013, background): “It has been found that EMT can confer stem-like properties on cells (61, 62).”
TGF-&bgr; signaling and epithelial–mesenchymal transition in cancer progression (2013, background): “Transformed human mammary epithelial cells that have undergone EMT show an increased ability to form mammospheres, soft agar colonies, and tumors, which correlates with their CSC properties [46,47].”
Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits (2009, background): “However, accumulating observations of human tumours and experimental animal models have provided convincing evidence for its physiological relevance to both normal embryogenesis and carcinogenesi”