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Cardamonin Suppresses TGF-β1-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, we examined, by Western blot, reverse transcriptio...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Society of Applied Pharmacology
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4354315/ https://www.ncbi.nlm.nih.gov/pubmed/25767682 http://dx.doi.org/10.4062/biomolther.2014.117 |
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author | Kim, Eun Ji Kim, Hyun Ji Park, Mi Kyung Kang, Gyeung Jin Byun, Hyun Jung Lee, Ho Lee, Chang Hoon |
author_facet | Kim, Eun Ji Kim, Hyun Ji Park, Mi Kyung Kang, Gyeung Jin Byun, Hyun Jung Lee, Ho Lee, Chang Hoon |
author_sort | Kim, Eun Ji |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4354315 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | The Korean Society of Applied Pharmacology |
record_format | MEDLINE/PubMed |
spelling | pubmed-43543152015-03-12 Cardamonin Suppresses TGF-β1-Induced Epithelial Mesenchymal Transition via Restoring Protein Phosphatase 2A Expression Kim, Eun Ji Kim, Hyun Ji Park, Mi Kyung Kang, Gyeung Jin Byun, Hyun Jung Lee, Ho Lee, Chang Hoon Biomol Ther (Seoul) Original Article 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. The Korean Society of Applied Pharmacology 2015-03 2015-03-01 /pmc/articles/PMC4354315/ /pubmed/25767682 http://dx.doi.org/10.4062/biomolther.2014.117 Text en Copyright © 2015 The Korean Society of Applied Pharmacology http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Kim, Eun Ji Kim, Hyun Ji Park, Mi Kyung Kang, Gyeung Jin Byun, Hyun Jung Lee, Ho Lee, Chang Hoon Cardamonin Suppresses TGF-β1-Induced Epithelial Mesenchymal Transition via Restoring Protein Phosphatase 2A Expression |
title | Cardamonin Suppresses TGF-β1-Induced Epithelial Mesenchymal Transition via Restoring Protein Phosphatase 2A Expression |
title_full | Cardamonin Suppresses TGF-β1-Induced Epithelial Mesenchymal Transition via Restoring Protein Phosphatase 2A Expression |
title_fullStr | Cardamonin Suppresses TGF-β1-Induced Epithelial Mesenchymal Transition via Restoring Protein Phosphatase 2A Expression |
title_full_unstemmed | Cardamonin Suppresses TGF-β1-Induced Epithelial Mesenchymal Transition via Restoring Protein Phosphatase 2A Expression |
title_short | Cardamonin Suppresses TGF-β1-Induced Epithelial Mesenchymal Transition via Restoring Protein Phosphatase 2A Expression |
title_sort | cardamonin suppresses tgf-β1-induced epithelial mesenchymal transition via restoring protein phosphatase 2a expression |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4354315/ https://www.ncbi.nlm.nih.gov/pubmed/25767682 http://dx.doi.org/10.4062/biomolther.2014.117 |
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