Portal:CPTAC/Hallmark/Invasion
From WikiPathways
(Difference between revisions)
(Added descriptive summary) |
(added WP185) |
||
| Line 7: | Line 7: | ||
*[[Pathway:WP3932]] Focal Adhesion-PI3K-Akt-mTOR-signaling pathway | *[[Pathway:WP3932]] Focal Adhesion-PI3K-Akt-mTOR-signaling pathway | ||
*[[Pathway:WP4239]] EMT transition in Colorectal Cancer | *[[Pathway:WP4239]] EMT transition in Colorectal Cancer | ||
| + | *[[Pathway:WP185]] Integrin-mediated Cell Adhesion | ||
Revision as of 01:44, 5 December 2018
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)
- Pathway:WP3301 MFAP5-mediated ovarian cancer cell motility and invasiveness
- Pathway:WP3859 TGF-B Signaling in Thyroid Cells for Epithelial-Mesenchymal Transition
- Pathway:WP3969 H19 action Rb-E2F1 signaling and CDK-β-catenin activity
- Pathway:WP185 Integrin-mediated Cell Adhesion
- Pathway:WP3932 Focal Adhesion-PI3K-Akt-mTOR-signaling pathway
- Pathway:WP4239 EMT transition in Colorectal Cancer
- Pathway:WP185 Integrin-mediated Cell Adhesion
