scholarly journals Inhibition of PTP1B disrupts cell–cell adhesion and induces anoikis in breast epithelial cells

2017 ◽  
Vol 8 (5) ◽  
pp. e2769-e2769 ◽  
Author(s):  
Bylgja Hilmarsdottir ◽  
Eirikur Briem ◽  
Skarphedinn Halldorsson ◽  
Jennifer Kricker ◽  
Sævar Ingthorsson ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Epithelial Cells ◽  
Breast Epithelial Cells ◽  
Breast Epithelial ◽  
Cell Cell

scholarly journals NCAM and attached polysialic acid affect behaviors of breast epithelial cells through differential signaling pathways

2020 ◽  
Author(s):  
Lin Cao ◽  
Xin Wang ◽  
Juhong Yang ◽  
Jia Guo ◽  
Xiang Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Adhesion ◽  
Epithelial Cells ◽  
Functional Role ◽  
Polysialic Acid ◽  
Breast Epithelial Cells ◽  
Differential Signaling ◽  
Breast Epithelial

Abstract Background Neural cell adhesion molecule (NCAM), a common mammalian cell surface glycoprotein, is the major substrate of polysialic acid (PSA). Polysialylated NCAM occurs in many types of cancer, but rarely in normal adult tissues. Epithelial-mesenchymal transition (EMT) is an important process contributing to tumor metastasis. The functional role of NCAM hypersialylation in EMT is unclear. Method Expression of NCAM and PSA-NCAM in breast cancer progression were evaluated by western blot (WB), immunohistochemistry, semi-quantitative PCR and immunoprecipitation (IP). Overexpression of NCAM-140 and STX were performed to assess the functional role of NCAM hypersialylation by liposome transfection. Then, the cell proliferation ability was investigated with MTT assay. Transwell and wound closure assay were conducted to evaluate cell migratory ability. Phagokinetic gold sol assay and cell adhesion assay were performed to assess cell motility ability and cell adhesion ability, respectively. Furthermore, WB and IP were used to reveal the activated signaling pathway. Results The present study indicates that NCAM and attached polysialic acid affect behaviors of breast epithelial cells through differential signaling pathways, based on the following observations: (i) NCAM and PSA-NCAM were aberrantly regulated in breast cancer cells; (ii) NCAM and PSA-NCAM expression were upregulated in normal breast epithelial cells undergoing EMT; (iii) NCAM overexpression induced EMT in breast epithelial cells; (iv) NCAM promoted cell proliferation and migration through activation of a β-catenin/slug signaling pathway; (v) modification of PSA attached to NCAM inhibited cell adhesion and promoted cell motility through activation of an EGFR/STAT3 pathway. Conclusion These observations help clarify the molecular mechanisms whereby PSA and its major substrate NCAM modulate cell behaviors, and the significance of increased PSA expression on NCAM during EMT and tumor development.

scholarly journals NCAM and attached polysialic acid affect behaviors of breast epithelial cells through differential signaling pathways

2020 ◽  
Author(s):  
Lin Cao ◽  
Xin Wang ◽  
Juhong Yang ◽  
Jia Guo ◽  
Xiang Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Functional Role ◽  
Polysialic Acid ◽  
Breast Epithelial Cells ◽  
Differential Signaling ◽  
Breast Epithelial

Abstract Background Neural cell adhesion molecule (NCAM), a common mammalian cell surface glycoprotein, is the major substrate of polysialic acid (polySia). Polysialylated NCAM occurs in many types of cancer, but rarely in normal adult tissues. Epithelial-mesenchymal transition (EMT) is an important process contributing to tumor metastasis. The functional role of NCAM hypersialylation in EMT is unclear. Method Expression of NCAM and polysialylated NCAM in breast cancer progression were evaluated by western blot (WB), immunohistochemistry, semi-quantitative PCR and immunoprecipitation (IP). Overexpression of NCAM-140 and ST8SiaII were performed to assess the functional role of NCAM hypersialylation by liposome transfection. Cell proliferation ability was investigated with MTT assay. Transwell and wound closure assay were conducted to evaluate cell migratory ability. Phagokinetic gold sol assay and cell adhesion assay were performed to assess cell motility ability and cell adhesion ability, respectively. Furthermore, WB and IP were used to reveal the activated signaling pathway. Results The present study indicates that NCAM and attached polysialic acid affect behaviors of breast epithelial cells through differential signaling pathways, based on the following observations: (i) NCAM and polysialylated NCAM were aberrantly regulated in breast cancer cells; (ii) NCAM and polysialylated NCAM expression were upregulated in normal breast epithelial cells undergoing EMT; (iii) NCAM overexpression induced EMT in breast epithelial cells; (iv) NCAM promoted cell proliferation and migration through activation of a β-catenin/slug signaling pathway; (v) modification of polySia attached to NCAM inhibited cell adhesion and promoted cell motility through activation of an EGFR/STAT3 pathway. Conclusion This study demonstrates that NCAM and polysialylated NCAM facilitate different signaling pathway and affect different cell behaviors. Switching between the NCAM-mediated pathways appeared to depend on polySia decoration.

scholarly journals NCAM and attached polysialic acid affect behaviors of breast epithelial cells through differential signaling pathways

2020 ◽  
Author(s):  
Lin Cao ◽  
Xin Wang ◽  
Juhong Yang ◽  
Jia Guo ◽  
Xiang Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Functional Role ◽  
Polysialic Acid ◽  
Breast Epithelial Cells ◽  
Differential Signaling ◽  
Breast Epithelial

Abstract Background Neural cell adhesion molecule (NCAM), a common mammalian cell surface glycoprotein, is the major substrate of polysialic acid (polySia). Polysialylated NCAM occurs in many types of cancer, but rarely in normal adult tissues. Epithelial-mesenchymal transition (EMT) is an important process contributing to tumor metastasis. The functional role of NCAM hypersialylation in EMT is unclear. Method Expression of NCAM and polysialylated NCAM in breast cancer progression were evaluated by western blot (WB), immunohistochemistry, semi-quantitative PCR and immunoprecipitation (IP). Overexpression of NCAM-140 and ST8SiaII were performed to assess the functional role of NCAM hypersialylation by liposome transfection. Cell proliferation ability was investigated with MTT assay. Transwell and wound closure assay were conducted to evaluate cell migratory ability. Phagokinetic gold sol assay and cell adhesion assay were performed to assess cell motility ability and cell adhesion ability, respectively. Furthermore, WB and IP were used to reveal the activated signaling pathway. Results The present study indicates that NCAM and attached polysialic acid affect behaviors of breast epithelial cells through differential signaling pathways, based on the following observations: (i) NCAM and polysialylated NCAM were aberrantly regulated in breast cancer cells; (ii) NCAM and polysialylated NCAM expression were upregulated in normal breast epithelial cells undergoing EMT; (iii) NCAM overexpression induced EMT in breast epithelial cells; (iv) NCAM promoted cell proliferation and migration through activation of a β-catenin/slug signaling pathway; (v) modification of polySia attached to NCAM inhibited cell adhesion and promoted cell motility through activation of an EGFR/STAT3 pathway.Conclusion This study demonstrates that NCAM and polysialylated NCAM facilitate different signaling pathway and affect different cell behaviors. Switching between the NCAM-mediated pathways appeared to depend on polySia decoration.

scholarly journals Loss of Tpm4.1 leads to disruption of cell-cell adhesions and invasive behavior in breast epithelial cells via increased Rac1 signaling

Oncotarget ◽  
2017 ◽  
Vol 8 (20) ◽  
pp. 33544-33559 ◽  
Author(s):  
SukYeong Jeong ◽  
SunYoung Lim ◽  
Galina Schevzov ◽  
Peter W. Gunning ◽  
David M. Helfman
Keyword(s):  
Epithelial Cells ◽  
Breast Epithelial Cells ◽  
Invasive Behavior ◽  
Breast Epithelial ◽  
Cell Adhesions ◽  
Cell Cell
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