ErbB receptor signalling in MCF7 breast cancer cells: an information theoretic approach

2019 ◽  
Author(s):  
Robert JP Pope ◽  
Gavin I Welsh ◽  
Richard J M Coward ◽  
Craig A McArdle
2010 ◽  
Vol 8 (1) ◽  
pp. 27-36 ◽  
Author(s):  
Imran H. Khan ◽  
Jing Zhao ◽  
Paramita Ghosh ◽  
Melanie Ziman ◽  
Colleen Sweeney ◽  
...  

2010 ◽  
Author(s):  
Scott J. Dawsey ◽  
Kathleen M. Woods Ignatoski ◽  
Kathleen C. Day

2006 ◽  
Vol 26 (3) ◽  
pp. 831-842 ◽  
Author(s):  
Chengfeng Yang ◽  
Ying Liu ◽  
Mark A. Lemmon ◽  
Marcelo G. Kazanietz

ABSTRACT Heregulins are a family of ligands for the ErbB3/ErbB4 receptors that play important roles in breast cancer cell proliferation and tumorigenesis. Limited information is available on the contribution of Rho GTPases to heregulin-mediated signaling. In breast cancer cells, heregulin β1 (HRG) causes a strong activation of Rac; however, it does so with striking differences in kinetics compared to epidermal growth factor, which signals through ErbB1 (epidermal growth factor receptor [EGFR]). Using specific ErbB receptor inhibitors and depletion of receptors by RNA interference (RNAi), we established that, surprisingly, activation of Rac by HRG is mediated not only by ErbB3 and ErbB2 but also by transactivation of EGFR, and it is independent of ErbB4. Similar receptor requirements are observed for HRG-induced actin cytoskeleton reorganization and mitogenic activity via extracellular signal-regulated kinase (ERK). HRG-induced Rac activation was phosphatidylinositol 3-kinase dependent and Src independent. Furthermore, inactivation of Rac by expression of the Rac GTPase-activating protein β2-chimerin inhibited HRG-induced ERK activation, mitogenicity, and migration in breast cancer cells. HRG mitogenic activity was also impaired by depletion of Rac1 using RNAi. Our studies established that Rac is a critical mediator of HRG mitogenic signaling in breast cancer cells and highlight additional levels of complexity for ErbB receptor coupling to downstream effectors that control aberrant proliferation and transformation.


2007 ◽  
Vol 120 (19) ◽  
pp. 3395-3403 ◽  
Author(s):  
J. Pu ◽  
C. D. McCaig ◽  
L. Cao ◽  
Z. Zhao ◽  
J. E. Segall ◽  
...  

Molecules ◽  
2021 ◽  
Vol 26 (21) ◽  
pp. 6661
Author(s):  
Olga E. Andreeva ◽  
Danila V. Sorokin ◽  
Ekaterina I. Mikhaevich ◽  
Irina V. Bure ◽  
Yuri Y. Shchegolev ◽  
...  

Hormone therapy is one of the most effective breast cancer treatments, however, its application is limited by the progression of hormonal resistance, both primary or acquired. The development of hormonal resistance is caused either by an irreversible block of hormonal signalling (suppression of the activity or synthesis of hormone receptors), or by activation of oestrogen-independent signalling pathways. Recently the effect of exosome-mediated intercellular transfer of hormonal resistance was revealed, however, the molecular mechanism of this effect is still unknown. Here, the role of exosomal miRNAs (microRNAs) in the transferring of hormonal resistance in breast cancer cells has been studied. The methods used in the work include extraction, purification and RNAseq of miRNAs, transfection of miRNA mimetics, immunoblotting, reporter analysis and the MTT test. Using MCF7 breast cancer cells and MCF7/T tamoxifen-resistant sub-line, we have found that some miRNAs, suppressors of oestrogen receptor signalling, are overexpressed in the exosomes of the resistant breast cancer cells. The multiple (but not single) transfection of one of the identified miRNA, miR-181a-2, into oestrogen-dependent MCF7 cells induced the irreversible tamoxifen resistance associated with the continuous block of the oestrogen receptor signalling and the activation of PI3K/Akt pathway. We suppose that the miRNAs-ERα suppressors may act as trigger agents inducing the block of oestrogen receptor signalling and breast cancer cell transition to an aggressive oestrogen-independent state.


Author(s):  
Tereza Nehybova ◽  
Jan Smarda ◽  
Lukas Daniel ◽  
Jan Brezovsky ◽  
Petr Benes

2010 ◽  
Vol 34 (8) ◽  
pp. S49-S49
Author(s):  
Lei Wang ◽  
Xun Zhou ◽  
Lihong Zhou ◽  
Yong Chen ◽  
Xun Zhu ◽  
...  

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