Cardamonin Suppresses TGF-b1-Induced Epithelial Mesenchymal Transition via Restoring Protein Phosphatase 2A Expression

Cardamonin Suppresses TGF-b1-Induced Epithelial Mesenchymal Transition via Restoring Protein Phosphatase 2A Expression

Epithelial mesenchymal transition (EMT) is the first step in metastasis and implicated in the phenotype of cancer stem cells. Therefore, understanding and controlling EMT, are essential to the prevention and cure of metastasis. In the present study, weexamined, by Western blot, reverse transcription polymerase chain reaction (RT-PCR), and confocal microscopy, the effects ofcardamonin (CDN) on transforming growth factor-b1 (TGF-b1)-induced EMT of A549 lung adenocarcinoma cell lines. TGF-b1 inducedexpression of N-cadherin and decreased expression of E-cadherin. CDN suppressed N-cadherin expression and restoredE-cadherin expression. Further, TGF-b1 induced migration and invasion of A549 cancer cells, which was suppressed by CDN. TGF-b1 induced c-Jun N-terminal kinase (JNK) activation during EMT, but CDN blocked it. Protein serine/threonine phosphatase2A (PP2A) expression in A549 cancer cells was reduced by TGF-b1 but CDN restored it. The overall data suggested that CDNsuppresses TGF-b1-induced EMT via PP2A restoration, making it a potential new drug candidate that controls metastasis.

Epithelial mesenchymal transition (EMT) is the first step in metastasis and implicated in the phenotype of cancer stem cells. Therefore, understanding and controlling EMT, are essential to the prevention and cure of metastasis. In the present study, weexamined, by Western blot, reverse transcription polymerase chain reaction (RT-PCR), and confocal microscopy, the effects ofcardamonin (CDN) on transforming growth factor-b1 (TGF-b1)-induced EMT of A549 lung adenocarcinoma cell lines. TGF-b1 inducedexpression of N-cadherin and decreased expression of E-cadherin. CDN suppressed N-cadherin expression and restoredE-cadherin expression. Further, TGF-b1 induced migration and invasion of A549 cancer cells, which was suppressed by CDN. TGF-b1 induced c-Jun N-terminal kinase (JNK) activation during EMT, but CDN blocked it. Protein serine/threonine phosphatase2A (PP2A) expression in A549 cancer cells was reduced by TGF-b1 but CDN restored it. The overall data suggested that CDNsuppresses TGF-b1-induced EMT via PP2A restoration, making it a potential new drug candidate that controls metastasis.