scholarly journals FER kinase promotes breast cancer metastasis by regulating α6- and β1-integrin-dependent cell adhesion and anoikis resistance

Oncogene ◽  
2013 ◽  
Vol 32 (50) ◽  
pp. 5582-5592 ◽  
Author(s):  
I A Ivanova ◽  
J F Vermeulen ◽  
C Ercan ◽  
J M Houthuijzen ◽  
F A Saig ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Β1 Integrin ◽  
Anoikis Resistance ◽  
Dependent Cell

Dietary Lipids, Cell Adhesion and Breast Cancer Metastasis

2002 ◽  
Author(s):  
Michael J. Toborek ◽  
Bernard Hennig ◽  
Larry W. Robertson
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Dietary Lipids

scholarly journals lncRNA APOC1P1-3 promoting anoikis-resistance of breast cancer cells

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Qi Lu ◽  
Li Wang ◽  
Yabiao Gao ◽  
Ping Zhu ◽  
Luying Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cancer Metastasis ◽  
Critical Role ◽  
Systemic Circulation ◽  
Breast Cancer Metastasis ◽  
Breast Cancer Cell Lines ◽  
Anoikis Resistance ◽  
Apoptosis Protein

Abstract Background Anoikis resistance plays a critical role in the tumor metastasis by allowing survival of cancer cells in the systemic circulation. We previously showed that long non-coding RNAs APOC1P1-3 (lncRNA APOC1P1-3) inhibit apoptosis of breast cancer cells. In this study, we explored its role in anoikis resistance. Methods We induced anoikis resistance in two breast cancer cell lines (MCF-7 and MDA-MB-231) under anchorage-independent culture conditions and studied lncRNA APOC1P1-3 effects on apoptosis. Using Dual-Luciferase activity assay, we determined whether it specifically binds to miRNA-188-3P. We further explored its role in lung metastasis by injecting MDA-MB-231 and MDA-MB-231-APOC1P1-3-knock-down cells in female BALB/c nude mice. Results We found that lncRNA APOC1P1-3 suppressed early apoptosis of these cells (demonstrated by gain or loss of their function, respectively) and promoted anoikis resistance via reducing activated- Caspase 3, 8, 9 and PARP. Moreover, it specifically binds to the target miRNA-188-3p acting as a “sponge” to block the inhibition of Bcl-2 (an anti-apoptosis protein). Conclusions Our study supports a theory that lncRNA APOC1P1-3 can promote development of breast cancer metastasis via anoikis resistance by specifically binding to miRNA-188-3p to block the inhibition of Bcl-2.

scholarly journals Targeted inactivation of β1 integrin induces β3 integrin switching, which drives breast cancer metastasis by TGF-β

2013 ◽  
Vol 24 (21) ◽  
pp. 3449-3459 ◽  
Author(s):  
Jenny G. Parvani ◽  
Amy J. Galliher-Beckley ◽  
Barbara J. Schiemann ◽  
William P. Schiemann
Keyword(s):  
Breast Cancer ◽  
Cancer Metastasis ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Breast Cancer Metastasis ◽  
Β1 Integrin ◽  
Metastatic Progression ◽  
Breast Cancer Patients ◽  
Mesenchymal Transition ◽  
Β3 Integrin

Mammary tumorigenesis and epithelial–mesenchymal transition (EMT) programs cooperate in converting transforming growth factor-β (TGF-β) from a suppressor to a promoter of breast cancer metastasis. Although previous reports associated β1 and β3 integrins with TGF-β stimulation of EMT and metastasis, the functional interplay and plasticity exhibited by these adhesion molecules in shaping the oncogenic activities of TGF-β remain unknown. We demonstrate that inactivation of β1 integrin impairs TGF-β from stimulating the motility of normal and malignant mammary epithelial cells (MECs) and elicits robust compensatory expression of β3 integrin solely in malignant MECs, but not in their normal counterparts. Compensatory β3 integrin expression also 1) enhances the growth of malignant MECs in rigid and compliant three-dimensional organotypic cultures and 2) restores the induction of the EMT phenotypes by TGF-β. Of importance, compensatory expression of β3 integrin rescues the growth and pulmonary metastasis of β1 integrin–deficient 4T1 tumors in mice, a process that is prevented by genetic depletion or functional inactivation of β3 integrin. Collectively our findings demonstrate that inactivation of β1 integrin elicits metastatic progression via a β3 integrin–specific mechanism, indicating that dual β1 and β3 integrin targeting is necessary to alleviate metastatic disease in breast cancer patients.

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