Metastatic colonization requires the repression of the epithelial-mesenchymal transition inducer Prrx1.

By Oscar H. Ocaña, R. Córcoles, A. Fabra, Gema Moreno-Bueno, H. Acloque, Sonia Vega, Alejandro Barrallo-Gimeno, A. Cano, M. Nieto. Cancer Cell, 2012

964 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/9a269b1cb379b6a8260ec3809ad290f990d8e6e9

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. R. Weinberg
2. M. Nieto
3. Jing Yang
4. J. Massagué
5. Thomas Brabletz
6. J. P. Thiery
7. Zena Werb
8. D. Pattabiraman

In Oncology

1. R. Weinberg
2. M. Nieto
3. J. Massagué
4. D. Pattabiraman
5. Jing Yang
6. Thomas Brabletz
7. J. P. Thiery
8. Zena Werb

Citations in the corpus

• EMT subtype influences epithelial plasticity and mode of cell migration (2018, background): “In cancer, EMT has been observed in murine tumor models where it has been proposed to play a role in invasion, hematogenous dissemination, and chemoresistance (Jolly et al., 2017; Lamouille et al., 2014; Nieto et al., 2016; Ocana et al., 2012; Rhim et al., 2012; Savagner, 2015; Shah et al., 2007; Ts”
• Epithelial Plasticity: A Common Theme in Embryonic and Cancer Cells (2013, background): “Indeed, malignancy by cancer cells require the reversion to the epithelial phenotype and the maintenance of a “stemness” state (70), which may be achieved when the Prrx1-type of EMT-TFs is repressed (16) and/or when”
• Epithelial-mesenchymal transition spectrum quantification and its efficacy in deciphering survival and drug responses of cancer patients (2014, positive): “Furthermore, even though EMT is often linked with the acquisition of stem cell-like features, Prrx1 uncouples EMT and stemness, resulting in a drug-resistant, metastatic colonization (Ocana et al , 2012).”
• Epithelial-Mesenchymal Plasticity: A central regulator of cancer progression (2015, background): “…several reports using different tumor models or cell line systems have converged on the conclusion that constitutive activation of strong EMT programs will block MET, and prevent colonization of tumor cells at the metastatic sites (Ocana et al., 2012; Stankic et al., 2013; Tsai et al., 2012).”
• The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis (2022, methodology): “This model is supported by several lines of evidence from studies of sphere formation and tumorigenicity in prostate and breast cancer models [6, 221, 268, 274].”
• Metastatic Stem Cells: Sources, Niches, and Vital Pathways (2014, background): “Although EMT favors the emigration of carcinoma cells from the primary tumor, it inhibits cell proliferation and interferes with the initiation of metastatic outgrowth (Ocaña et al., 2012; Stankic et al., 2013; Tsai et al., 2012; Celià-Terrassa et al., 2012).”
• Extracellular Matrix in the Tumor Microenvironment and Its Impact on Cancer Therapy (2020, background): “EMT is linked not only to increased metastasis (Yang et al., 2004; Mani et al., 2007; Ocana et al., 2012; Stankic et al., 2013) but also to chemoresistance (Singh and Settleman, 2010; Haslehurst et al.”