scholarly journals EGF receptor signalling is essential for electric-field-directed migration of breast cancer cells

2007 ◽  
Vol 120 (19) ◽  
pp. 3395-3403 ◽  
Author(s):  
J. Pu ◽  
C. D. McCaig ◽  
L. Cao ◽  
Z. Zhao ◽  
J. E. Segall ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Electric Field ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Egf Receptor ◽  
Directed Migration ◽  
Receptor Signalling

scholarly journals Chemotaxis model for human breast cancer cells based on signal-to-noise ratio

2018 ◽  
Author(s):  
S. Lim ◽  
H. Nam ◽  
J.S. Jeon
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cancer Metastasis ◽  
Egf Receptor ◽  
Signal To Noise Ratio ◽  
Signal To Noise ◽  
Biological Phenomena ◽  
Organ Specific ◽  
Noise Ratio

ABSTRACTChemotaxis, a biased migration of cells under a chemical gradient, plays a significant role in diverse biological phenomena including cancer metastasis. Stromal cells release signaling proteins to induce chemotaxis, which further causes organ-specific metastasis. Epidermal growth factor (EGF) is an example of the chemical attractants, and its gradient stimulates metastasis of breast cancer cells. Hence, the interactions between EGF and breast cancer cells have long been a subject of interest for oncologists and clinicians. However, most current approaches do not systematically separate the effects of gradient and absolute concentration of EGF on chemotaxis of breast cancer cells. In this work, we develop a theoretical model based on signal-to-noise ratio to represent stochastic properties and report our microfluidic experiments to verify the analytical predictions from the model. The results demonstrate that even under the same EGF concentration gradients, breast cancer cells can reveal distinct chemotaxis patterns at different absolute concentrations. Moreover, we found that addition of EGF receptor antibody can promote chemotaxis at a low EGF level. This apparently counterintuitive finding suggests that EGF receptor-targeted therapy may stimulate metastasis of breast cancer at a particular condition, which should be considered in anticancer drug design.

Kisspeptin-10 inhibits bone-directed migration of GPR54-positive breast cancer cells: Evidence for a dose–window effect

2010 ◽  
Vol 119 (3) ◽  
pp. 571-578 ◽  
Author(s):  
Teresa Olbrich ◽  
Elke Ziegler ◽  
Gregor Türk ◽  
Antje Schubert ◽  
Günter Emons ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Directed Migration ◽  
Window Effect ◽  
Positive Breast Cancer

scholarly journals Parthenolide induces superoxide anion production by stimulating EGF receptor in MDA-MB-231 breast cancer cells

2013 ◽  
Vol 43 (6) ◽  
pp. 1895-1900 ◽  
Author(s):  
A. D’ANNEO ◽  
D. CARLISI ◽  
S. EMANUELE ◽  
G. BUTTITTA ◽  
R. DI FIORE ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Superoxide Anion ◽  
Breast Cancer Cells ◽  
Egf Receptor ◽  
Superoxide Anion Production ◽  
Anion Production

scholarly journals AXL Controls Directed Migration of Mesenchymal Triple-Negative Breast Cancer Cells

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 247 ◽  
Author(s):  
Olivier Zajac ◽  
Renaud Leclere ◽  
André Nicolas ◽  
Didier Meseure ◽  
Caterina Marchiò ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Golgi Apparatus ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Leading Edge ◽  
Luminal Breast Cancer ◽  
Directed Migration

Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer with high risk of relapse and metastasis. TNBC is a heterogeneous disease comprising different molecular subtypes including those with mesenchymal features. The tyrosine kinase AXL is expressed in mesenchymal cells and plays a role in drug resistance, migration and metastasis. We confirm that AXL is more expressed in mesenchymal TNBC cells compared to luminal breast cancer cells, and that its invalidation impairs cell migration while having no or little effect on cell viability. Here, we found that AXL controls directed migration. We observed that AXL displays a polarized localization at the Golgi apparatus and the leading edge of migratory mesenchymal TNBC cells. AXL co-localizes with F-actin at the front of the cells. In migratory polarized cells, the specific AXL inhibitor R428 displaces AXL and F-actin from the leading edge to a lateral area localized between the front and the rear of the cells where both are enriched in protrusions. In addition, R428 treatment disrupts the polarized localization of the Golgi apparatus towards the leading edge in migratory cells. Immunohistochemical analysis of aggressive chemo-resistant TNBC samples obtained before treatment reveals inter- and intra-tumor heterogeneity of the percentage of AXL expressing tumor cells, and a preference of these cells to be in contact with the stroma. Taken together, our study demonstrates that AXL controls directed cell migration most likely by regulating cell polarity.

scholarly journals Estrogen Negatively Regulates Epidermal Growth Factor (EGF)-Mediated Signal Transducer and Activator of Transcription 5 Signaling in Human EGF Family Receptor-Overexpressing Breast Cancer Cells

2005 ◽  
Vol 19 (11) ◽  
pp. 2660-2670 ◽  
Author(s):  
Julie L. Boerner ◽  
Matthew A. Gibson ◽  
Emily M. Fox ◽  
Erika D. Posner ◽  
Sarah J. Parsons ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factors ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Egf Receptor ◽  
Signal Transducer ◽  
Epidermal Growth ◽  
Egf Family

Abstract Breast cancer cell growth may be stimulated by 17β-estradiol (E2) or growth factors like epidermal growth factor (EGF). However, tumors typically depend on only one of these pathways and may overexpress either estrogen receptor (ER) or EGF receptor (EGFR) and related family members. Tumors overexpressing EGFR are more aggressive than those expressing ER. Intracellular mediators of these growth-stimulatory pathways are not completely defined, but one potential common mediator of EGF and E2 signaling is the transcription factor signal transducer and activator of transcription 5 (STAT5). To investigate the role of STAT5 in potential crosstalk between E2 and EGF, MDA-MB231 and SKBr3 breast cancer cells, which are ER-negative and overexpress human EGF family receptors, were used. Introduction of ERα and treatment with E2 decreased EGF-induced tyrosine phosphorylation of STAT5b, basal and EGF-induced STAT5-mediated transcription, and EGF-stimulated DNA synthesis in these cells. Suppressive effects of E2-ΕRα were specific for STAT5, as EGF stimulation of MAPK was unaffected. Deletion/mutation analysis of ERα demonstrated that the DNA-binding domain was insufficient, and that the ligand-binding domain was required for these responses. ERα transcriptional activity was not necessary for suppression of STAT5 activity. Overexpression of c-Src did not prevent suppression of STAT5 activity by E2 and ERα. However, ERα did prevent basal increases in STAT5 activity with overexpressed c-Src. In the context of human EGF receptor family overexpression, E2-ER opposes EGF signaling by regulating STAT5 activity. STAT5 may be a crucial point of signaling for both E2 and growth factors in breast cancer cells, allowing targeted therapy for many types of breast tumors.

Nanoparticle Mediated Thermal Ablation of Breast Cancer Cells Using a Nanosecond Pulsed Electric Field

2013 ◽  
Vol 12 (2) ◽  
pp. 112-118 ◽  
Author(s):  
Christopher D. Burford ◽  
K. D. Bhattacharyya ◽  
N. Boriraksantikul ◽  
P. J. D. Whiteside ◽  
B. P. Robertson ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Electric Field ◽  
Cancer Cells ◽  
Thermal Ablation ◽  
Breast Cancer Cells ◽  
Pulsed Electric Field ◽  
Nanosecond Pulsed Electric Field

scholarly journals Amphiregulin retains ERα expression in acquired aromatase inhibitor resistant breast cancer cells

2020 ◽  
Vol 27 (12) ◽  
pp. 671-683
Author(s):  
Yuanzhong Wang ◽  
Yen-Dun Tony Tzeng ◽  
Gregory Chang ◽  
Xiaoqiang Wang ◽  
Shiuan Chen
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Egf Receptor ◽  
Acquired Resistance ◽  
Endocrine Resistance ◽  
Ectopic Expression ◽  
Clinical Issue ◽  
Forkhead Box M1 ◽  
Estrogen Production

Acquired resistance to aromatase inhibitors (AIs) is a significant clinical issue in endocrine therapy for estrogen receptor (ER) positive breast cancer which accounts for the majority of breast cancer. Despite estrogen production being suppressed, ERα signaling remains active and plays a key role in most AI-resistant breast tumors. Here, we found that amphiregulin (AREG), an ERα transcriptional target and EGF receptor (EGFR) ligand, is crucial for maintaining ERα expression and signaling in acquired AI-resistant breast cancer cells. AREG was deregulated and critical for cell viability in ER+ AI-resistant breast cancer cells, and ectopic expression of AREG in hormone responsive breast cancer cells promoted endocrine resistance. RNA-sequencing and reverse phase protein array analyses revealed that AREG maintains ERα expression and signaling by activation of PI3K/Akt/mTOR signaling and upregulation of forkhead box M1 (FOXM1) and serum- and glucocorticoid-inducible kinase 3 (SGK3) expression. Our study uncovers a previously unappreciated role of AREG in maintaining ERα expression and signaling, and establishes the AREG-ERα crosstalk as a driver of acquired AI resistance in breast cancer.

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