Cardamonin Suppresses TGF-beta1-Induced Epithelial Mesenchymal Transition via Restoring Protein Phosphatase 2A Expression.
10.4062/biomolther.2014.117
- Author:
Eun Ji KIM
1
;
Hyun Ji KIM
;
Mi Kyung PARK
;
Gyeung Jin KANG
;
Hyun Jung BYUN
;
Ho LEE
;
Chang Hoon LEE
Author Information
1. BK21PLUS R-FIND Team, College of Pharmacy, Dongguk University, Seoul 100-715, Republic of Korea. uatheone@dongguk.edu
- Publication Type:Original Article
- Keywords:
Cardamonin;
Epithelial mesenchymal transition;
TGF-beta1;
JNK;
PP2A;
A549
- MeSH:
Adenocarcinoma;
Blotting, Western;
Cadherins;
Cell Line;
Epithelial-Mesenchymal Transition*;
JNK Mitogen-Activated Protein Kinases;
Lung;
Microscopy, Confocal;
Neoplasm Metastasis;
Neoplastic Stem Cells;
Phenotype;
Polymerase Chain Reaction;
Protein Phosphatase 2*;
Reverse Transcription;
Transforming Growth Factor beta1
- From:Biomolecules & Therapeutics
2015;23(2):141-148
- CountryRepublic of Korea
- Language:English
-
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-beta1 (TGF-beta1)-induced EMT of A549 lung adenocarcinoma cell lines. TGF-beta1 induced expression of N-cadherin and decreased expression of E-cadherin. CDN suppressed N-cadherin expression and restored E-cadherin expression. Further, TGF-beta1 induced migration and invasion of A549 cancer cells, which was suppressed by CDN. TGF-beta1 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-beta1 but CDN restored it. The overall data suggested that CDN suppresses TGF-beta1-induced EMT via PP2A restoration, making it a potential new drug candidate that controls metastasis.
