Wnt/β-catenin signaling in cancer stemness and malignant behavior

By R. Fodde, Thomas Brabletz. 2007

723 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/839ef46cb4893f126364ad772d2d7e8de0b0c7d1

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In Molecular Biology

In Oncology

Citations in the corpus

Epithelial—mesenchymal and mesenchymal—epithelial transitions in carcinoma progression (2007, background): “In colon cancer, constitutive activation of the Wnt signaling pathway is a key contributor to tumorigenesis (reviewed in Fodde and Brabletz, 2007).”
E-cadherin, β-catenin, and ZEB1 in malignant progression of cancer (2009, neutral): “as survivin and MDR [176–181].”
Cadherins and cancer: how does cadherin dysfunction promote tumor progression? (2008, background): “Furthermore, canonical Wnt signaling is often upregulated in tumors (Fodde and Brabletz, 2007).”
A double-negative feedback loop between ZEB1-SIP1 and the microRNA-200 family regulates epithelial-mesenchymal transition. (2008, background): “For example, mutation of the APC gene in colorectal cancer leads to nuclear h-catenin localization and signaling, facilitating subsequent EMT-like processes (37).”
Epithelial-mesenchymal transition: at the crossroads of development and tumor metastasis. (2008, background): “More interestingly, tumor cells with nuclear b-catenin accumulation appear to have undergone an EMT, as demonstrated by the progressive loss of E-cadherin expression and acquisition of mesenchymal markers such as fibronectin (Fodde and Brabletz, 2007).”
Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “In the absence of signaling, β-catenin is phosphorylated by a complex of GSK-3β, Axin, and the tumor suppressor adenomatous polyposis coli (APC), which sequesters β-catenin in the cytoplasm and marks it for proteasomal degradation (165).”