scholarly journals Positive Cross-Talk Between CXC Chemokine Receptor 4 (CXCR4) and Epidermal Growth Factor Receptor (EGFR) Promotes Gastric Cancer Metastasis via the Nuclear Factor kappa B (NF-kB)-Dependent Pathway

2020 ◽  
Vol 26 ◽  
Author(s):  
Yu Cheng ◽  
Xiaofang Che ◽  
Simeng Zhang ◽  
Tianshu Guo ◽  
Xin He ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Nuclear Factor Kappa B ◽  
Cancer Metastasis ◽  
Growth Factor Receptor ◽  
Nuclear Factor ◽  
Cxc Chemokine Receptor 4 ◽  
Cxc Chemokine ◽  
Epidermal Growth ◽  
Chemokine Receptor 4 ◽  
Dependent Pathway

Minecoside Modulates Cell Invasion via Regulation of CXCR4 Expression in Breast and Colon Cancer Cells

Planta Medica ◽  
2020 ◽  
Vol 86 (05) ◽  
pp. 331-337
Author(s):  
Buyun Kim ◽  
Yu-Hong Min ◽  
Byoungduck Park
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Chemokine Receptor ◽  
Cancer Metastasis ◽  
Transcriptional Level ◽  
Cxc Chemokine Receptor 4 ◽  
Cxc Chemokine ◽  
Cancer Cell Survival ◽  
Organ Specific ◽  
Chemokine Receptor 4

AbstractMetastasis, which is closely linked to cancer-related deaths, is a highly complex process. It is an organ-specific process and involves interactions between the host and cancer cells. CXC chemokine receptor 4 is known to be expressed in various tumors and the binding with CXC ligand 12 induces signaling in cancer cell survival, migration, and proliferation. Particularly, the CXC chemokine receptor 4/CXC ligand 12 axis is known to promote the metastasis of breast cancer. Thus, agents that can downregulate CXC chemokine receptor 4 expression have potential against cancer metastasis. Minecoside is an active compound extracted from Veronica peregrina L. It is widely distributed in Korea and has been used as a traditional drug for the treatment of various chronic diseases. However, the anticancer and anti-inflammatory effects of minecoside have yet to be clarified. In this study, we found that minecoside downregulates constitutive CXC chemokine receptor 4 expression in MDA-MB-231 breast cancer cells. This downregulation also occurred at the transcriptional level. Minecoside-mediated suppression of CXC chemokine receptor 4 expression inhibited CXC ligand 12-induced invasion of breast and colorectal cancer cells. Overall, our results suggest that minecoside can be a novel anticancer agent that can inhibit cancer metastasis through inhibition of CXC chemokine receptor 4 expression.

scholarly journals β-arrestin mediates communication between plasma membrane and intracellular GPCRs to regulate signaling

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Maxwell S. DeNies ◽  
Alan V. Smrcka ◽  
Santiago Schnell ◽  
Allen P. Liu
Keyword(s):  
Plasma Membrane ◽  
Molecular Mechanisms ◽  
Cancer Metastasis ◽  
Cxc Chemokine Receptor 4 ◽  
Gpcr Activation ◽  
Cxc Chemokine ◽  
Cationic Channel ◽  
Highly Correlated ◽  
Chemokine Receptor 4 ◽  
G Protein Coupled

AbstractIt has become increasingly apparent that G protein-coupled receptor (GPCR) localization is a master regulator of cell signaling. However, the molecular mechanisms involved in this process are not well understood. To date, observations of intracellular GPCR activation can be organized into two categories: a dependence on OCT3 cationic channel-permeable ligands or the necessity of endocytic trafficking. Using CXC chemokine receptor 4 (CXCR4) as a model, we identified a third mechanism of intracellular GPCR signaling. We show that independent of membrane permeable ligands and endocytosis, upon stimulation, plasma membrane and internal pools of CXCR4 are post-translationally modified and collectively regulate EGR1 transcription. We found that β-arrestin-1 (arrestin 2) is necessary to mediate communication between plasma membrane and internal pools of CXCR4. Notably, these observations may explain that while CXCR4 overexpression is highly correlated with cancer metastasis and mortality, plasma membrane localization is not. Together these data support a model where a small initial pool of plasma membrane-localized GPCRs are capable of activating internal receptor-dependent signaling events.

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