GEP100 links epidermal growth factor receptor signalling to Arf6 activation to induce breast cancer invasion

@article{Morishige2008GEP100LE,
  title={GEP100 links epidermal growth factor receptor signalling to Arf6 activation to induce breast cancer invasion},
  author={Masaki Morishige and Shigeru Hashimoto and E. Ogawa and Yoshinobu Toda and Hirokazu Kotani and Mayumi Hirose and Shu-li Wei and Ari Hashimoto and Atsuko Yamada and Hajime Yano and Yuichi Mazaki and Hiroshi Kodama and Yoshinori Nio and Toshiaki Manabe and Hiromi Wada and Hidenori Kobayashi and Hisataka Sabe},
  journal={Nature Cell Biology},
  year={2008},
  volume={10},
  pages={85-92}
}
Epidermal growth factor (EGF) receptor (EGFR) signalling is implicated in tumour invasion and metastasis. However, whether there are EGFR signalling pathways specifically used for tumour invasion still remains elusive. Overexpression of Arf6 and its effector, AMAP1, correlates with and is crucial for the invasive phenotypes of different breast cancer cells. Here we identify the mechanism by which Arf6 is activated to induce tumour invasion. We found that GEP100/BRAG2, a guanine nucleotide… 
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Signalling: The GEP100 pathway to invasion
TLDR
It is reported that the ADP-ribosylation factor (ARF) guanine nucleotide-exchange factor (GEF) ARFGEP100 induces breast cancer invasion by specifically activating the GTPase ARF6 in response to EGF.
The EGFR-GEP100-Arf6 pathway in breast cancer
TLDR
The results reveal an aspect of the precise molecular mechanism of cancer invasion and metastasis, in which full invasiveness is not acquired just by alterations of cancer cells themselves, but their microenvironments may also play pivotal roles.
The EGFR-GEP100-Arf6-AMAP1 Signaling Pathway Specific to Breast Cancer Invasion and Metastasis†
TLDR
The results reveal an aspect of the precise molecular mechanisms of some breast cancers, in which full invasiveness is not acquired just by intracellular alterations of cancer cells, but extracellular factors from microenvironments may also be necessary.
Epidermal Growth Factor Receptor-GEP100-Arf6 Axis Affects the Prognosis of Lung Adenocarcinoma
TLDR
The EGFR-GEP100-Arf6 axis affected the prognosis of patients with primary lung adenocarcinoma, and the combination of p-EGFR, GEP100, and Arf6 staining can predict the prog outlook of patients after surgery.
GEP100 regulates epidermal growth factor-induced MDA-MB-231 breast cancer cell invasion through the activation of Arf6/ERK/uPAR signaling pathway.
The Adaptor Proteins p66Shc and Grb2 Regulate the Activation of the GTPases ARF1 and ARF6 in Invasive Breast Cancer Cells*
TLDR
A central role is identified for adaptor proteins p66Shc and Grb2 in the regulation of ARF1 and ARF6 activation in invasive breast cancer cells and an important role is shown in modulating ARF activation, cell growth, and migration in HER2-positive breast cancer Cells.
GEP100-Arf6-AMAP1-Cortactin Pathway Frequently Used in Cancer Invasion Is Activated by VEGFR2 to Promote Angiogenesis
TLDR
It is demonstrated that the same GEP100-Arf6-AMAP1-cortactin pathway is essential for angiogenesis activities, including cell migration and tubular formation, as well as for the enhancement of cell permeability and VE-cadherin endocytosis of VEGF-stimulated HUVECs.
GEP100/Arf6 Is Required for Epidermal Growth Factor-Induced ERK/Rac1 Signaling and Cell Migration in Human Hepatoma HepG2 Cells
TLDR
This study highlights the function of the PH domain of GEP100 and its regulated Arf6/ERK/Rac1 signaling cascade in EGF-induced hepatoma cell migration and could provide a rationale for designing new therapy based on inhibition of hepatoma metastasis.
GEP 100-Arf 6-AMAP 1-Cortactin Pathway Frequently Used in Cancer Invasion Is Activated by VEGFR 2 to Promote Angiogenesis
TLDR
It is demonstrated that the same GEP100-Arf6-AMAP1-cortactin pathway is essential for angiogenesis activities, including cell migration and tubular formation, as well as for the enhancement of cell permeability and VE-cadherin endocytosis of VEGF-stimulated HUVECs.
ADP-ribosylation factor 1 expression regulates epithelial-mesenchymal transition and predicts poor clinical outcome in triple-negative breast cancer
TLDR
The findings demonstrate that ARF1 is a molecular switch for cancer progression and thus suggest that limiting the expression/activation of this GTPase could help improve outcome for breast cancer patients.
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