ERBB-2 overexpression confers PI 3 ′ kinase-dependent invasion capacity on human mammary epithelial cells
| Autor: | Kathleen M. Woods Ignatoski, Tomohiko Maehama, Donna L. Livant, Jack E. Dixon, Stephen P. Ethier, Sonja Markwart |
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| Jazyk: | angličtina |
| Rok vydání: | 2000 |
| Předmět: |
Cancer Research
Cell Survival medicine.medical_treatment Breast Neoplasms Biology medicine.disease_cause Focal adhesion Phosphatidylinositol 3-Kinases ErbB P13′ kinase medicine PTEN Humans Neoplasm Invasiveness Breast skin and connective tissue diseases human breast cancer ERBB-2 Growth factor Cancer Regular Article Genes erbB-2 medicine.disease invasion human mammary epithelial cells Phenotype Oncology Cell culture Cancer cell Immunology biology.protein Cancer research Carcinogenesis Cell Division Signal Transduction |
| Zdroj: | British Journal of Cancer |
| ISSN: | 1532-1827 0007-0920 |
| Popis: | Amplification and overexpression of ERBB-2 in human breast cancer is thought to play a significant role in the progression of the disease; however, its precise role in the aetiology of altered phenotypes associated with human breast cancer is unknown. We have previously shown that exogenous overexpression of ERBB-2 conferred growth factor independence on human mammary epithelial cells. In this study, we show that ERBB-2 overexpression also causes the cells to acquire other characteristics exhibited by human breast cancer cells, such as anchorage-independent growth and invasion capabilities. ERBB-2-induced invasion is dependent on fibronectin and correlates with the down-regulation of cell surface α4 integrin. In addition ERBB-2 co-immunoprecipitates with focal adhesion kinase (FAK) in these cells. We have also shown, by use of exogenously expressed PTEN and by treatment with the PI3′-kinase inhibitor LY294002, that ERBB-2-induced invasion is dependent on the PI3′-kinase pathway; however, PTEN does not dephosphorylate FAK in these cells. © 2000 Cancer Research Campaign |
| Databáze: | OpenAIRE |
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