Cell-Cell Adhesion and Breast Cancer.

1998 ◽  
Author(s):  
Stephen W. Byers
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Cell Cell

Phosphatidylinositol 4-Phosphate in the Golgi Apparatus Regulates Cell–Cell Adhesion and Invasive Cell Migration in Human Breast Cancer

2014 ◽  
Vol 74 (11) ◽  
pp. 3054-3066 ◽  
Author(s):  
Emi Tokuda ◽  
Toshiki Itoh ◽  
Junya Hasegawa ◽  
Takeshi Ijuin ◽  
Yukiko Takeuchi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cell Adhesion ◽  
Golgi Apparatus ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Phosphatidylinositol 4 ◽  
Invasive Cell ◽  
Cell Cell

scholarly journals Role of the Protein Tyrosine Kinase Syk in Regulating Cell-Cell Adhesion and Motility in Breast Cancer Cells

2009 ◽  
Vol 7 (5) ◽  
pp. 634-644 ◽  
Author(s):  
Xiaoying Zhang ◽  
Ulka Shrikhande ◽  
Bethany M. Alicie ◽  
Qing Zhou ◽  
Robert L. Geahlen
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Tyrosine Kinase ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Protein Tyrosine Kinase ◽  
Protein Tyrosine ◽  
Cell Cell

scholarly journals Parsing β-catenin’s cell adhesion and Wnt signaling functions in malignant mammary tumor progression

2021 ◽  
Vol 118 (34) ◽  
pp. e2020227118
Author(s):  
David Buechel ◽  
Nami Sugiyama ◽  
Natalia Rubinstein ◽  
Meera Saxena ◽  
Ravi K. R. Kalathur ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Wnt Signaling ◽  
Tumor Progression ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Mammary Tumor ◽  
Dual Function ◽  
Mammary Tumor Cells ◽  
Cell Cell

During malignant progression, epithelial cancer cells dissolve their cell–cell adhesion and gain invasive features. By virtue of its dual function, β-catenin contributes to cadherin-mediated cell–cell adhesion, and it determines the transcriptional output of Wnt signaling: via its N terminus, it recruits the signaling coactivators Bcl9 and Pygopus, and via the C terminus, it interacts with the general transcriptional machinery. This duality confounds the simple loss-of-function analysis of Wnt signaling in cancer progression. In many cancer types including breast cancer, the functional contribution of β-catenin’s transcriptional activities, as compared to its adhesion functions, to tumor progression has remained elusive. Employing the mouse mammary tumor virus (MMTV)–PyMT mouse model of metastatic breast cancer, we compared the complete elimination of β-catenin with the specific ablation of its signaling outputs in mammary tumor cells. Notably, the complete lack of β-catenin resulted in massive apoptosis of mammary tumor cells. In contrast, the loss of β-catenin’s transcriptional activity resulted in a reduction of primary tumor growth, tumor invasion, and metastasis formation in vivo. These phenotypic changes were reflected by stalled cell cycle progression and diminished epithelial–mesenchymal transition (EMT) and cell migration of breast cancer cells in vitro. Transcriptome analysis revealed subsets of genes which were specifically regulated by β-catenin’s transcriptional activities upon stimulation with Wnt3a or during TGF-β–induced EMT. Our results uncouple the signaling from the adhesion function of β-catenin and underline the importance of Wnt/β-catenin–dependent transcription in malignant tumor progression of breast cancer.

scholarly journals Keratin 19 maintains E-cadherin localization at the cell surface and stabilizes cell-cell adhesion of MCF7 cells

2020 ◽  
Author(s):  
Sarah Alsharif ◽  
Pooja Sharma ◽  
Karina Bursch ◽  
Rachel Milliken ◽  
Meagan Collins ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cell Adhesion ◽  
Cell Mechanics ◽  
Mcf7 Cells ◽  
Growth And Survival ◽  
Recycling Endosomes ◽  
Keratin 19 ◽  
E Cadherin ◽  
Cell Cell

AbstractA cytoskeletal protein keratin 19 (K19) is highly expressed in breast cancer but its effects on breast cancer cell mechanics are unclear. Using KRT19 knockout (KO) cells and cells where K19 expression was rescued, we found that K19 is required to maintain rounded epithelial-like shape and tight cell-cell adhesion of MCF7 cells. A loss of K19 resulted in a lower level of plakoglobin and internalization of E-cadherin in early and recycling endosomes. Inhibiting internalization restored cell-cell adhesion of KRT19 KO cells, suggesting E-cadherin internalization contributes to defective adhesion. Ultimately, while K19 inhibited cell migration, it was required for cells to form colonies in suspension. Our results suggest that K19 stabilizes E-cadherin complexes at the cell membrane to maintain cell-cell adhesion which inhibits cell migration but provides growth and survival advantages for circulating tumor cells. These findings provide context-dependent roles of K19 during metastasis.

scholarly journals Cell–cell adhesion and 3D matrix confinement determine jamming transitions in breast cancer invasion

2020 ◽  
Vol 22 (9) ◽  
pp. 1103-1115 ◽  
Author(s):  
Olga Ilina ◽  
Pavlo G. Gritsenko ◽  
Simon Syga ◽  
Jürgen Lippoldt ◽  
Caterina A. M. La Porta ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Cancer Invasion ◽  
Breast Cancer Invasion ◽  
3D Matrix ◽  
Cell Cell
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