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, we examined, by Western blot, reverse transcription polymerase chain reaction (RT-PCR), and confocal microscopy, the effects of
cardamonin (CDN) on transforming growth factor-β1 (TGF-β1)-induced EMT of A549
lung adenocarcinoma cell lines. TGF-β1 induced expression of
N-cadherin and decreased expression of
E-cadherin. CDN suppressed
N-cadherin expression and restored
E-cadherin expression. Further, TGF-β1 induced migration and invasion of A549
cancer cells, which was suppressed by CDN. TGF-β1 induced
c-Jun N-terminal kinase (JNK) activation during EMT, but CDN blocked it.
Protein serine/threonine phosphatase 2A (PP2A) expression in A549
cancer cells was reduced by TGF-β1 but CDN restored it. The overall data suggested that CDN suppresses TGF-β1-induced EMT via PP2A restoration, making it a potential new
drug candidate that controls
metastasis.