Cardamonin suppresses TGF-β1-induced epithelial mesenchymal transition via restoring protein phosphatase 2A expression

Eun Ji Kim, Hyun Ji Kim, Mi Kyung Park, Gyeung Jin Kang, Hyun Jung Byun, Ho Lee, Chang Hoon Lee, Chang Hoon Lee

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

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-b1 (TGF-b1)-induced EMT of A549 lung adenocarcinoma cell lines. TGF-b1 induced expression of N-cadherin and decreased expression of E-cadherin. CDN suppressed N-cadherin expression and restored E-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 phosphatase 2A (PP2A) expression in A549 cancer cells was reduced by TGF-b1 but CDN restored it. The overall data suggested that CDN suppresses TGF-b1-induced EMT via PP2A restoration, making it a potential new drug candidate that controls metastasis.

Original languageEnglish (US)
Pages (from-to)141-148
Number of pages8
JournalBiomolecules and Therapeutics
Volume23
Issue number2
DOIs
StatePublished - Mar 1 2015

Keywords

  • A549
  • Cardamonin
  • Epithelial mesenchymal transition
  • JNK
  • PP2A
  • TGF-b1

Fingerprint Dive into the research topics of 'Cardamonin suppresses TGF-β1-induced epithelial mesenchymal transition via restoring protein phosphatase 2A expression'. Together they form a unique fingerprint.

Cite this