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

doi:10.4062/biomolther.2014.117

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

Medicine - Cardiology Division

Research output: Contribution to journal › Article › peer-review

20 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 language	English (US)
Pages (from-to)	141-148
Number of pages	8
Journal	Biomolecules and Therapeutics
Volume	23
Issue number	2
DOIs	https://doi.org/10.4062/biomolther.2014.117
State	Published - Mar 1 2015

Bibliographical note

Publisher Copyright:
© 2015 The Korean Society of Applied Pharmacology

Keywords

A549
Cardamonin
Epithelial mesenchymal transition
JNK
PP2A
TGF-b1

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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

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.",

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

Abstract

Bibliographical note

Keywords

UN SDGs

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