EPHA5 mutation impairs natural killer cell-mediated cytotoxicity against non-small lung cancer cells and promotes cancer cell migration and invasion

2020 ◽  
Vol 52 ◽  
pp. 101566 ◽  
Author(s):  
Jingwen Zhang ◽  
Zhihao Zhang ◽  
Weiwei Song ◽  
Jumin Liu
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Natural Killer Cell ◽  
Cancer Cells ◽  
Natural Killer ◽  
Cancer Cell ◽  
Killer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Cell Migration And Invasion

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.

Rab22a enhances CD147 recycling and is required for lung cancer cell migration and invasion

2017 ◽  
Vol 357 (1) ◽  
pp. 9-16 ◽  
Author(s):  
Yang Zhou ◽  
Bo Wu ◽  
Jiang-Hua Li ◽  
Gang Nan ◽  
Jian-Li Jiang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Lung Cancer Cell ◽  
Cell Migration And Invasion

scholarly journals Regulation of Lung Cancer Cell Migration and Invasion by Reactive Oxygen Species and Caveolin-1

2010 ◽  
Vol 285 (50) ◽  
pp. 38832-38840 ◽  
Author(s):  
Sudjit Luanpitpong ◽  
Siera Jo Talbott ◽  
Yon Rojanasakul ◽  
Ubonthip Nimmannit ◽  
Varisa Pongrakhananon ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Reactive Oxygen Species ◽  
Cell Migration ◽  
Cancer Cell ◽  
Migration And Invasion ◽  
Oxygen Species ◽  
Cancer Cell Migration ◽  
Lung Cancer Cell ◽  
Cell Migration And Invasion ◽  
Caveolin 1

scholarly journals The C-Terminus Tail Regulates ERK3 Kinase Activity and Its Ability in Promoting Cancer Cell Migration and Invasion

2020 ◽  
Vol 21 (11) ◽  
pp. 4044 ◽  
Author(s):  
Lobna Elkhadragy ◽  
Hadel Alsaran ◽  
Weiwen Long
Keyword(s):  
Cell Migration ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Molecular Mechanisms ◽  
Kinase Activity ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Cell Migration And Invasion ◽  
C Terminus

Extracellular signal-regulated kinase 3 (ERK3) is an atypical member of the mitogen-activated protein kinase (MAPK) family. It harbors a kinase domain in the N-terminus and a long C-terminus extension. The C-terminus extension comprises a conserved in ERK3 and ERK4 (C34) region and a unique C-terminus tail, which was shown to be required for the interaction of ERK3 with the cytoskeletal protein septin 7. Recent studies have elucidated the role of ERK3 signaling in promoting the motility and invasiveness of cancer cells. However, little is known about the intramolecular regulation of the enzymatic activity and cellular functions of ERK3. In this study, we investigated the role of the elongated C-terminus extension in regulating ERK3 kinase activity and its ability to promote cancer cell migration and invasion. Our study revealed that the deletion of the C-terminus tail greatly diminishes the ability of ERK3 to promote the migration and invasion of lung cancer cells. We identified two molecular mechanisms underlying this effect. Firstly, the deletion of the C-terminus tail decreases the kinase activity of ERK3 towards substrates, including the oncogenic protein steroid receptor co-activator 3 (SRC-3), an important downstream target for ERK3 signaling in cancer. Secondly, in line with the previous finding that the C-terminus tail mediates the interaction of ERK3 with septin 7, we found that the depletion of septin 7 abolished the ability of ERK3 to promote migration, indicating that septin 7 acts as a downstream effector for ERK3-induced cancer cell migration. Taken together, the findings of this study advance our understanding of the molecular regulation of ERK3 signaling by unraveling the role of the C-terminus tail in regulating ERK3 kinase activity and functions in cancer cells. These findings provide useful insights for the development of therapeutic agents targeting ERK3 signaling in cancer.

scholarly journals MKL1 potentiates lung cancer cell migration and invasion by epigenetically activating MMP9 transcription

Oncogene ◽  
2015 ◽  
Vol 34 (44) ◽  
pp. 5570-5581 ◽  
Author(s):  
X Cheng ◽  
Y Yang ◽  
Z Fan ◽  
L Yu ◽  
H Bai ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Lung Cancer Cell ◽  
Cell Migration And Invasion
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