Variable β-catenin expression in colorectal cancers indicates tumor progression driven by the tumor environment

By Thomas Brabletz, A. Jung, S. Reu, M. Porzner, F. Hlubek, Leoni A. Kunz-Schughart, R. Knuechel, T. Kirchner. Proceedings of the National Academy of Sciences of the United States of America, 2001

1,155 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/f47ae14201e6b8d1b7a7bc4ab53167e96cf536e5

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Citations in the corpus

Hallmarks of cancer: the next generation. (2011, neutral): “…suggests that heterotypic interactions of cancer cells with adjacent tumor-associated stromal cells can induce expression of the malignant cell phenotypes that are known to be choreographed by one or more of these transcriptional regulators (Karnoub and Weinberg, 2006–2007; Brabletz et al., 2001).”
Inflammation and EMT: an alliance towards organ fibrosis and cancer progression (2009, background): “This EMT–MET double switch for metastasis formation has been discussed by Brabletz et al (2001) while providing a convincing illustration of an EMT process at the invasive front of human colon carcinoma (Fig 2A).”
Epithelial-mesenchymal transition in cancer metastasis: mechanisms, markers and strategies to overcome drug resistance in the clinic. (2009, background): “In agreement, dedifferentiated mesenchyme-like tumour cells expressing nuclear β-catenin were found at the invasive front of a colorectal carcinoma but not in the subsequent metastatic tumour of epithelial morphology [124].”
E-cadherin, β-catenin, and ZEB1 in malignant progression of cancer (2009, background): “and recapitulate the morphology of the primary tumor, indicating a MET during metastasis formation [169].”
Epithelial Plasticity: A Common Theme in Embryonic and Cancer Cells (2013, background): “However, the differentiated phenotype of metastases reflects the epithelial plasticity implicated in tumor progression, in order words, the reversion of EMT firstly suggested by Brabletz and colleagues (43) and again resembling the situations described during embryonic development (34).”
The transcription factor ZEB1 (δEF1) promotes tumour cell dedifferentiation by repressing master regulators of epithelial polarity (2007, background): “As EMT-like phenotypic conversions at the tumour– host interface are prominent features of colorectal cancer progression (Brabletz et al., 2001, 2005), we screened tumour–host interfaces for ZEB1 expression.”
Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “The synthesis of fibronectin is also associated with Wnt activation and accumulation of nuclear β-catenin, providing further evidence of multiple signaling pathways converging to produce ECM capable of supporting migration (173).”
A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells (2008, background): “Metastases often recapitulate the differentiated phenotype of the primary tumour; therefore, EMT seems to be transiently activated by the inductive tumour environment at the invasive tumour edge, but is reversed in growing metastases (Brabletz et al, 2001, 2005).”
The ins and outs of APC and β‐catenin nuclear transport (2002, background): “These shifts in β-catenin localization may reflect changes in cadherins and the local cell microenvironment (Brabletz et al., 2001), although it is not known whether they involve changes in nuclear transport or anchorage.”
The ZEB/miR‐200 feedback loop—a motor of cellular plasticity in development and cancer? (2010, background): “…the EMt/stemness phenotype of tumour cells that favours dissemination is associated with a growth arrest of invasive and disseminating tumour cells (Brabletz et al, 2001; Jung et al, 2001; Vega et al, 2004), such tumour stem cells must consequently switch back to the differentiation and…”
Up-regulation of miR-200 and let-7 by natural agents leads to the reversal of epithelial-mesenchymal transition in gemcitabine-resistant pancreatic cancer cells (2009, neutral): “Studies have also shown that cancer cells in the tumor center remain positive for the expression of E-cadherin and cytoplasmic h-catenin; however, the tumor cells in the periphery with propensity for invasion display loss of surface E-cadherin and up-regulation of vimentin, the typical characteristi”