scholarly journals Caveolin-1 Up-regulation during Epithelial to Mesenchymal Transition Is Mediated by Focal Adhesion Kinase

2008 ◽  
Vol 283 (20) ◽  
pp. 13714-13724 ◽  
Author(s):  
Kelly M. Bailey ◽  
Jun Liu
Keyword(s):  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Caveolin 1

scholarly journals Artocarpin Targets Focal Adhesion Kinase-Dependent Epithelial to Mesenchymal Transition and Suppresses Migratory-Associated Integrins in Lung Cancer Cells

Pharmaceutics ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 554
Author(s):  
Nongyao Nonpanya ◽  
Kittipong Sanookpan ◽  
Nicharat Sriratanasak ◽  
Chanida Vinayanuwattikun ◽  
Duangdao Wichadakul ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Focal Adhesion Kinase ◽  
Cancer Cells ◽  
Focal Adhesion ◽  
Epithelial To Mesenchymal Transition ◽  
Epithelial Mesenchymal Transition ◽  
Lung Cancer Cells ◽  
Normal Lung ◽  
Mesenchymal Transition ◽  
Phosphorylated Akt

Focal adhesion kinase (FAK) controls several cancer aggressive potentials of cell movement and dissemination. As epithelial–mesenchymal transition (EMT) and the migratory-associated integrins, known influencers of metastasis, have been found to be linked with FAK activity, this study unraveled the potential pharmacological effect of artocarpin in targeting FAK resulting in the suppression of EMT and migratory behaviors of lung cancer cells. Treatment with artocarpin was applied at concentrations of 0–10 μM, and the results showed non-cytotoxicity in lung cancer cell lines (A549 and H460), normal lung (BEAS-2B) cells and primary metastatic lung cancer cells (ELC12, ELC16, and ELC20). We also found that artocarpin (0–10 µM) had no effect on cell viability, proliferation, and migration in BEAS-2B cells. For metastasis-related approaches, artocarpin significantly inhibited cell migration, invasion, and filopodia formation. Artocarpin also dramatically suppressed anchorage-independent growth, cancer stem cell (CSC) spheroid formation, and viability of CSC-rich spheroids. For molecular targets of artocarpin action, computational molecular docking revealed that artocarpin had the best binding affinity of −8.0 kcal/mol with FAK protein. Consistently, FAK-downstream proteins, namely active Akt (phosphorylated Akt), active mTOR (phosphorylated mTOR), and Cdc42, and EMT marker and transcription factor (N-cadherin, Vimentin, and Slug), were found to be significantly depleted in response to artocarpin treatment. Furthermore, we found the decrease of Caveolin-1 (Cav-1) accompanied by the reduction of integrin-αν and integrin-β3. Taken together, these findings support the anti-metastasis potentials of the compound to be further developed for cancer therapy.

scholarly journals Src- and confinement-dependent FAK activation causes E-cadherin relaxation and β-catenin activity

2018 ◽  
Vol 217 (3) ◽  
pp. 1063-1077 ◽  
Author(s):  
Charlène Gayrard ◽  
Clément Bernaudin ◽  
Théophile Déjardin ◽  
Cynthia Seiler ◽  
Nicolas Borghi
Keyword(s):  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Epithelial To Mesenchymal Transition ◽  
Nuclear Translocation ◽  
Nuclear Activity ◽  
Kinase Activation ◽  
Mesenchymal Transition ◽  
Cell Substrate ◽  
Quantitative Fluorescence ◽  
E Cadherin

In epithelia, E-cadherin cytoplasmic tail is under cytoskeleton-generated tension via a link that contains β-catenin. A cotranscription factor, β-catenin, is also active in morphogenetic processes associated with epithelial-to-mesenchymal transition. β-Catenin signaling appears mechanically inducible and was proposed to follow phosphorylation-induced β-catenin release from E-cadherin. Evidence for this mechanism is lacking, and whether E-cadherin tension is involved is unknown. To test this, we combined quantitative fluorescence microscopies with genetic and pharmacological perturbations of epithelial-to-mesenchymal transition–induced cells in culture. We showed that β-catenin nuclear activity follows a substantial release from the membrane specific to migrating cells and requires multicellular deconfinement and Src activity. Selective nuclear translocation occurs downstream of focal adhesion kinase activation, which targets E-cadherin tension relaxation through actomyosin remodeling. In contrast, phosphorylations of the cadherin/catenin complex are not substantially required. These data demonstrate that E-cadherin acts as a sensor of intracellular mechanics in a crosstalk with cell-substrate adhesions that target β-catenin signaling.

Focal adhesion kinase mediates TGF-β1-induced renal tubular epithelial-to-mesenchymal transition in vitro

2010 ◽  
Vol 340 (1-2) ◽  
pp. 21-29 ◽  
Author(s):  
Bingqing Deng ◽  
Xiao Yang ◽  
Jianshe Liu ◽  
Fangfang He ◽  
Zhonghua Zhu ◽  
...  
Keyword(s):  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Renal Tubular ◽  
Tgf Β1

Caveolin-1 promotes trophoblast cell invasion through the focal adhesion kinase (FAK) signalling pathway during early human placental development

2019 ◽  
Vol 31 (6) ◽  
pp. 1057 ◽  
Author(s):  
Zhihui Dai ◽  
Fei Sheng ◽  
Ningxia Sun ◽  
Yixuan Ji ◽  
Qiuying Liao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Cell Invasion ◽  
Trophoblast Cell ◽  
Signalling Pathway ◽  
Placental Development ◽  
Human Trophoblast ◽  
Expression Levels ◽  
Caveolin 1

Normal implantation and placental development depend on the appropriate differentiation and invasion of trophoblast cells. Inadequate trophoblast cell invasion results in pregnancy-related disorders, which endanger both mother and fetus; however, the mechanism of early placental development has not been fully explained. In this study we conducted gene expression profile analysis using mouse placental tissues at different developmental stages (embryonic day (E)7.5, E14.5 and E19.5) using series tests of cluster (STC) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway analyses. Focal adhesion kinase (FAK) signalling pathway-related gene expression levels were verified using quantitative reverse transcription polymerase chain reaction and western blot. The results showed that caveolin-1 (Cav1) was downregulated in the placenta of unexplained spontaneous abortion subjects compared with that of induced abortion. Furthermore, by modulating CAV1 expression levels, CAV1 was shown to promote human trophoblast cell proliferation, migration and invasion by activating the FAK signalling pathway. These results indicate that CAV1 and the FAK signalling pathway are crucial for early placental development, which sheds new light on our understanding of the mechanisms of human trophoblast cell invasion and early development of the placenta.

scholarly journals A ZIP6-ZIP10 heteromer controls NCAM1 phosphorylation and integration into focal adhesion complexes during epithelial-to-mesenchymal transition

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Dylan Brethour ◽  
Mohadeseh Mehrabian ◽  
Declan Williams ◽  
Xinzhu Wang ◽  
Farinaz Ghodrati ◽  
...  
Keyword(s):  
Focal Adhesion ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition

Curcumin ameliorates epithelial-to-mesenchymal transition of podocytes in vivo and in vitro via regulating caveolin-1

2014 ◽  
Vol 68 (8) ◽  
pp. 1079-1088 ◽  
Author(s):  
Li-na Sun ◽  
Zhi-xin Chen ◽  
Xiang-chun Liu ◽  
Hai-ying Liu ◽  
Guang-ju Guan ◽  
...  
Keyword(s):  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Caveolin 1

scholarly journals Cordycepin Suppresses Endothelial Cell Proliferation, Migration, Angiogenesis, and Tumor Growth by Regulating Focal Adhesion Kinase and p53

Cancers ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 168 ◽  
Author(s):  
Yi-Ting Lin ◽  
Shu-Man Liang ◽  
Ya-Ju Wu ◽  
Yi-Ju Wu ◽  
Yi-Jhu Lu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Tumor Growth ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Epithelial Mesenchymal Transition ◽  
Endothelial Cell Proliferation ◽  
Mice Model ◽  
Mesenchymal Transition

Focal adhesion kinase (FAK) plays an important role in vascular development, including the regulation of endothelial cell (EC) adhesion, migration, proliferation, and survival. 3’-deoxyadenosine (cordycepin) is known to suppress FAK expression, cell migration, and the epithelial–mesenchymal transition in hepatocellular carcinoma (HCC). However, whether cordycepin affects FAK expression and cellular functions in ECs and the specific molecular mechanism remain unclear. In this study, we found that cordycepin suppressed FAK expression and the phosphorylation of FAK (p-FAK) at Tyr397 in ECs. Cordycepin inhibited the proliferation, wound healing, transwell migration, and tube formation of ECs. Confocal microscopy revealed that cordycepin significantly reduced FAK expression and decreased focal adhesion number of ECs. The suppressed expression of FAK was accompanied by induced p53 and p21 expression in ECs. Finally, we demonstrated that cordycepin suppressed angiogenesis in an in vivo angiogenesis assay and reduced HCC tumor growth in a xenograft nude mice model. Our study indicated that cordycepin could attenuate cell proliferation and migration and may result in the impairment of the angiogenesis process and tumor growth via downregulation of FAK and induction of p53 and p21 in ECs. Therefore, cordycepin may be used as a potential adjuvant for cancer therapy.

Positioning of integrin β1, caveolin-1 and focal adhesion kinase on the adhered membrane of spreading cells

2013 ◽  
Vol 37 (12) ◽  
pp. 1276-1284 ◽  
Author(s):  
Špela Zemljič Jokhadar ◽  
Janja Majhenc ◽  
Saša Svetina ◽  
Urška Batista
Keyword(s):  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Integrin Β1 ◽  
Caveolin 1
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