scholarly journals Altered LKB1/CREB-regulated transcription co-activator (CRTC) signaling axis promotes esophageal cancer cell migration and invasion

Oncogene ◽  
2011 ◽  
Vol 31 (4) ◽  
pp. 469-479 ◽  
Author(s):  
Y Gu ◽  
S Lin ◽  
J-L Li ◽  
H Nakagawa ◽  
Z Chen ◽  
...  
Keyword(s):  
Esophageal Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Cell Migration And Invasion ◽  
Signaling Axis ◽  
Esophageal Cancer Cell

scholarly journals p62 is Negatively Implicated in the TRAF6-BECN1 Signaling Axis for Autophagy Activation and Cancer Progression by Toll-Like Receptor 4 (TLR4)

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1142 ◽  
Author(s):  
Mi-Jeong Kim ◽  
Yoon Min ◽  
Ji Seon Im ◽  
Juhee Son ◽  
Joo Sang Lee ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cancer Cells ◽  
Cancer Cell ◽  
A549 Cells ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Cell Migration And Invasion ◽  
Signaling Axis

Toll-like receptors (TLRs) induce the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and autophagy through the TNF (Tumor necrosis factor) receptor-associated factor 6 (TRAF6)-evolutionarily conserved signaling intermediate in Toll pathways (ECSIT) and TRAF6-BECN1 signaling axes, respectively. Having shown that p62 negatively regulates Toll-like receptor 4 (TLR4)-mediated signaling via TRAF6-ECSIT signaling axis, we herein investigated whether p62 is functionally implicated in the TRAF6-BECN1 signaling axis, thereby regulating cancer cell migration and invasion. p62 interacted with TRAF6 and BECN1, to interrupt the functional associations required for TRAF6-BECN1 complex formation, leading to inhibitions of BECN1 ubiquitination and autophagy activation. Importantly, p62-deficient cancer cells, such as p62-knockdown (p62KD) SK-HEP-1, p62KD MDA-MB-231, and p62-knockout (p62KO) A549 cells, showed increased activation of autophagy induced by TLR4 stimulation, suggesting that p62 negatively regulates autophagy activation. Moreover, these p62-deficient cancer cells exhibited marked increases in cell migration and invasion in response to TLR4 stimulation. Collectively, these results suggest that p62 is negatively implicated in the TRAF6-BECN1 signaling axis, thereby inhibiting cancer cell migration and invasion regulated by autophagy activation in response to TLR4 stimulation.

scholarly journals IL-24 Inhibits Lung Cancer Cell Migration and Invasion by Disrupting The SDF-1/CXCR4 Signaling Axis

PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0122439 ◽  
Author(s):  
Janani Panneerselvam ◽  
Jiankang Jin ◽  
Manish Shanker ◽  
Jason Lauderdale ◽  
Jonathan Bates ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Lung Cancer Cell ◽  
Cell Migration And Invasion ◽  
Cxcr4 Signaling ◽  
Signaling Axis

scholarly journals Thy-1 (CD90)-Induced Metastatic Cancer Cell Migration and Invasion Are β3 Integrin-Dependent and Involve a Ca2+/P2X7 Receptor Signaling Axis

2021 ◽  
Vol 8 ◽  
Author(s):  
Marianne Brenet ◽  
Samuel Martínez ◽  
Ramón Pérez-Nuñez ◽  
Leonardo A. Pérez ◽  
Pamela Contreras ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
P2x7 Receptor ◽  
Melanoma Cells ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Cell Migration And Invasion ◽  
Signaling Axis

Cancer cell adhesion to the vascular endothelium is an important step in tumor metastasis. Thy-1 (CD90), a cell adhesion molecule expressed in activated endothelial cells, has been implicated in melanoma metastasis by binding to integrins present in cancer cells. However, the signaling pathway(s) triggered by this Thy-1-Integrin interaction in cancer cells remains to be defined. Our previously reported data indicate that Ca2+-dependent hemichannel opening, as well as the P2X7 receptor, are key players in Thy-1-αVβ3 Integrin-induced migration of reactive astrocytes. Thus, we investigated whether this signaling pathway is activated in MDA-MB-231 breast cancer cells and in B16F10 melanoma cells when stimulated with Thy-1. In both cancer cell types, Thy-1 induced a rapid increase in intracellular Ca2+, ATP release, as well as cell migration and invasion. Connexin and Pannexin inhibitors decreased cell migration, implicating a requirement for hemichannel opening in Thy-1-induced cell migration. In addition, cell migration and invasion were precluded when the P2X7 receptor was pharmacologically blocked. Moreover, the ability of breast cancer and melanoma cells to transmigrate through an activated endothelial monolayer was significantly decreased when the β3 Integrin was silenced in these cancer cells. Importantly, melanoma cells with silenced β3 Integrin were unable to metastasize to the lung in a preclinical mouse model. Thus, our results suggest that the Ca2+/hemichannel/ATP/P2X7 receptor-signaling axis triggered by the Thy-1-αVβ3 Integrin interaction is important for cancer cell migration, invasion and transvasation. These findings open up the possibility of therapeutically targeting the Thy-1-Integrin signaling pathway to prevent metastasis.

Inhibition of cancer-cell migration by tetraspanin CD9-binding peptide

2021 ◽  
Author(s):  
Thanawat Suwatthanarak ◽  
Masayoshi Tanaka ◽  
Yoshitaka Miyamoto ◽  
Kenji Miyado ◽  
Mina Okochi
Keyword(s):  
Cell Migration ◽  
Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Binding Peptide ◽  
Cell Migration And Invasion ◽  
Inhibition Effect

A CD9-binding peptide (RSHRLRLH), screened from EWI-2, was characterized, and its inhibition effect on cancer-cell migration and invasion was demonstrated.

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