scholarly journals Direct regulation of transforming growth factor β‐induced epithelial–mesenchymal transition by the protein phosphatase activity of unphosphorylated PTEN in lung cancer cells

2015 ◽  
Vol 106 (12) ◽  
pp. 1693-1704 ◽  
Author(s):  
Masaaki Kusunose ◽  
Naozumi Hashimoto ◽  
Motohiro Kimura ◽  
Ryo Ogata ◽  
Daisuke Aoyama ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Growth Factor ◽  
Cancer Cells ◽  
Phosphatase Activity ◽  
Protein Phosphatase ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Transforming Growth Factor Β ◽  
Mesenchymal Transition ◽  
Direct Regulation

scholarly journals Vasohibin-2 is required for epithelial-mesenchymal transition of ovarian cancer cells by modulating transforming growth factor-β signaling

2017 ◽  
Vol 108 (3) ◽  
pp. 419-426 ◽  
Author(s):  
Rie Norita ◽  
Yasuhiro Suzuki ◽  
Yutaka Furutani ◽  
Kazuki Takahashi ◽  
Yasuhiro Yoshimatsu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Growth Factor ◽  
Cancer Cells ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Transforming Growth Factor Β ◽  
Ovarian Cancer Cells ◽  
Mesenchymal Transition

scholarly journals Inhibition of A549 Lung Cancer Cell Migration and Invasion by Ent-Caprolactin C via the Suppression of Transforming Growth Factor-β-Induced Epithelial—Mesenchymal Transition

Marine Drugs ◽  
2021 ◽  
Vol 19 (8) ◽  
pp. 465
Author(s):  
So Young Kim ◽  
Myoung-Sook Shin ◽  
Geum Jin Kim ◽  
Hyukbean Kwon ◽  
Myong Jin Lee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Growth Factor ◽  
Cancer Cell ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
A549 Cells ◽  
Transforming Growth Factor Β ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Mesenchymal Transition

The epithelial–mesenchymal transition (EMT) of cancer cells is a crucial process in cancer cell metastasis. An Aquimarina sp. MC085 extract was found to inhibit A549 human lung cancer cell invasion, and caprolactin C (1), a new natural product, α-amino-ε-caprolactam linked to 3-methyl butanoic acid, was purified through bioactivity-guided isolation of the extract. Furthermore, its enantiomeric compound, ent-caprolactin C (2), was synthesized. Both 1 and 2 inhibited the invasion and γ-irradiation-induced migration of A549 cells. In transforming growth factor-β (TGF-β)-treated A549 cells, 2 inhibited the phosphorylation of Smad2/3 and suppressed the EMT cell marker proteins (N-cadherin, β-catenin, and vimentin), as well as the related messenger ribonucleic acid expression (N-cadherin, matrix metalloproteinase-9, Snail, and vimentin), while compound 1 did not suppress Smad2/3 phosphorylation and the expression of EMT cell markers. Therefore, compound 2 could be a potential candidate for antimetastatic agent development, because it suppresses TGF-β-induced EMT.

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