Portal:CPTAC/Hallmark/Invasion

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Current revision (18:10, 10 October 2019) (view source)
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*[[Pathway:WP3997]]
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E-cadherin was well established as an antagonist of invasion and metastasis. The frequently observed downregulation and occasional mutational inactivation of E-cadherin in human carcinomas provided strong support for its role as a key suppressor of this hallmark capability. Additionally, expression of genes encoding other cell-to-cell and cell-to-ECM adhesion molecules is demonstrably altered in some highly aggressive carcinomas, with those favoring cytostasis typically being downregulated. Conversely, adhesion molecules normally associated with the cell migrations that occur during embryogenesis and inflammation are often upregulated. (Adapted from [https://www.ncbi.nlm.nih.gov/pubmed/21376230 Hallmarks of cancer: the next generation, Hanahan and Weinberg, Cell 2011])
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*[[Pathway:WP3980]]
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*[[Pathway:WP3624]]
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*[[Pathway:WP3301]] MFAP5-mediated ovarian cancer cell motility and invasiveness
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*[[Pathway:WP3632]]
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*[[Pathway:WP3859]] TGF-B Signaling in Thyroid Cells for Epithelial-Mesenchymal Transition
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*[[Pathway:WP4010]]
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*[[Pathway:WP3969]] H19 action Rb-E2F1 signaling and CDK-β-catenin activity
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*[[Pathway:WP4011]]
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*[[Pathway:WP185]] Integrin-mediated Cell Adhesion
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*[[Pathway:WP4017]]
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*[[Pathway:WP3932]] Focal Adhesion-PI3K-Akt-mTOR-signaling pathway
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*[[Pathway:WP4026]]
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*[[Pathway:WP4239]] EMT transition in Colorectal Cancer
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*[[Pathway:WP185]] Integrin-mediated Cell Adhesion
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*[[Pathway:WP4565]] Neural Crest Cell Migration in Cancer

Current revision

E-cadherin was well established as an antagonist of invasion and metastasis. The frequently observed downregulation and occasional mutational inactivation of E-cadherin in human carcinomas provided strong support for its role as a key suppressor of this hallmark capability. Additionally, expression of genes encoding other cell-to-cell and cell-to-ECM adhesion molecules is demonstrably altered in some highly aggressive carcinomas, with those favoring cytostasis typically being downregulated. Conversely, adhesion molecules normally associated with the cell migrations that occur during embryogenesis and inflammation are often upregulated. (Adapted from Hallmarks of cancer: the next generation, Hanahan and Weinberg, Cell 2011)

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