Piperlongumine Inhibits Migration of Glioblastoma Cells via Activation of ROS-Dependent p38 and JNK Signaling Pathways
Piperlongumine (PL) is recently found to kill cancer cells selectively and effectively via targeting reactive oxygen species (ROS) responses. To further explore the therapeutic effects of PL in cancers, we investigated the role and mechanisms of PL in cancer cell migration....
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Format: | Article |
Language: | English |
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Hindawi Limited
2014-01-01
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Series: | Oxidative Medicine and Cellular Longevity |
Online Access: | http://dx.doi.org/10.1155/2014/653732 |
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record_format |
Article |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Qian Rong Liu Ju Mei Liu Yong Chen Xiao Qiang Xie Xin Xin Xiong Xin Yao Qiu Feng Pan Di Liu Shang Bin Yu Xiao Qian Chen |
spellingShingle |
Qian Rong Liu Ju Mei Liu Yong Chen Xiao Qiang Xie Xin Xin Xiong Xin Yao Qiu Feng Pan Di Liu Shang Bin Yu Xiao Qian Chen Piperlongumine Inhibits Migration of Glioblastoma Cells via Activation of ROS-Dependent p38 and JNK Signaling Pathways Oxidative Medicine and Cellular Longevity |
author_facet |
Qian Rong Liu Ju Mei Liu Yong Chen Xiao Qiang Xie Xin Xin Xiong Xin Yao Qiu Feng Pan Di Liu Shang Bin Yu Xiao Qian Chen |
author_sort |
Qian Rong Liu |
title |
Piperlongumine Inhibits Migration of Glioblastoma Cells via Activation of ROS-Dependent p38 and JNK Signaling Pathways |
title_short |
Piperlongumine Inhibits Migration of Glioblastoma Cells via Activation of ROS-Dependent p38 and JNK Signaling Pathways |
title_full |
Piperlongumine Inhibits Migration of Glioblastoma Cells via Activation of ROS-Dependent p38 and JNK Signaling Pathways |
title_fullStr |
Piperlongumine Inhibits Migration of Glioblastoma Cells via Activation of ROS-Dependent p38 and JNK Signaling Pathways |
title_full_unstemmed |
Piperlongumine Inhibits Migration of Glioblastoma Cells via Activation of ROS-Dependent p38 and JNK Signaling Pathways |
title_sort |
piperlongumine inhibits migration of glioblastoma cells via activation of ros-dependent p38 and jnk signaling pathways |
publisher |
Hindawi Limited |
series |
Oxidative Medicine and Cellular Longevity |
issn |
1942-0900 1942-0994 |
publishDate |
2014-01-01 |
description |
Piperlongumine (PL) is recently found to kill cancer cells selectively and effectively via targeting reactive oxygen species (ROS) responses.
To further explore the therapeutic effects of PL in cancers, we investigated the role and mechanisms of PL in cancer cell migration.
PL effectively inhibited the migration of human glioma (LN229 or U87 MG) cells but not normal astrocytes in the scratch-wound culture model.
PL did not alter EdU+-cells and cdc2, cdc25c, or cyclin D1 expression in our model.
PL increased ROS (measured by DCFH-DA), reduced glutathione, activated p38 and JNK, increased IκBα,
and suppressed NFκB in LN229 cells after scratching.
All the biological effects of PL in scratched LN229 cells were completely abolished by the antioxidant N-acetyl-L-cysteine (NAC).
Pharmacological administration of specific p38 (SB203580) or JNK (SP600125) inhibitors significantly reduced the inhibitory effects of
PL on LN229 cell migration and NFκB activity in scratch-wound and/or transwell models. PL prevented the deformation of migrated LN229 cells while NAC,
SB203580, or SP600125 reversed PL-induced morphological changes of migrated cells.
These results suggest potential therapeutic effects of PL in the treatment and prevention of highly malignant tumors such as glioblastoma multiforme (GBM)
in the brain by suppressing tumor invasion and metastasis. |
url |
http://dx.doi.org/10.1155/2014/653732 |
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doaj-8659b719bfc5491a9a8c8a9237c9e6cd2020-11-24T23:07:18ZengHindawi LimitedOxidative Medicine and Cellular Longevity1942-09001942-09942014-01-01201410.1155/2014/653732653732Piperlongumine Inhibits Migration of Glioblastoma Cells via Activation of ROS-Dependent p38 and JNK Signaling PathwaysQian Rong Liu0Ju Mei Liu1Yong Chen2Xiao Qiang Xie3Xin Xin Xiong4Xin Yao Qiu5Feng Pan6Di Liu7Shang Bin Yu8Xiao Qian Chen9Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Neurological Diseases, Ministry of Education and Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, ChinaDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Neurological Diseases, Ministry of Education and Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, ChinaDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Neurological Diseases, Ministry of Education and Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, ChinaDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Neurological Diseases, Ministry of Education and Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, ChinaDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Neurological Diseases, Ministry of Education and Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, ChinaDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Neurological Diseases, Ministry of Education and Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, ChinaDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Neurological Diseases, Ministry of Education and Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, ChinaDepartment of Urology, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, ChinaDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Neurological Diseases, Ministry of Education and Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, ChinaDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Neurological Diseases, Ministry of Education and Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, ChinaPiperlongumine (PL) is recently found to kill cancer cells selectively and effectively via targeting reactive oxygen species (ROS) responses. To further explore the therapeutic effects of PL in cancers, we investigated the role and mechanisms of PL in cancer cell migration. PL effectively inhibited the migration of human glioma (LN229 or U87 MG) cells but not normal astrocytes in the scratch-wound culture model. PL did not alter EdU+-cells and cdc2, cdc25c, or cyclin D1 expression in our model. PL increased ROS (measured by DCFH-DA), reduced glutathione, activated p38 and JNK, increased IκBα, and suppressed NFκB in LN229 cells after scratching. All the biological effects of PL in scratched LN229 cells were completely abolished by the antioxidant N-acetyl-L-cysteine (NAC). Pharmacological administration of specific p38 (SB203580) or JNK (SP600125) inhibitors significantly reduced the inhibitory effects of PL on LN229 cell migration and NFκB activity in scratch-wound and/or transwell models. PL prevented the deformation of migrated LN229 cells while NAC, SB203580, or SP600125 reversed PL-induced morphological changes of migrated cells. These results suggest potential therapeutic effects of PL in the treatment and prevention of highly malignant tumors such as glioblastoma multiforme (GBM) in the brain by suppressing tumor invasion and metastasis.http://dx.doi.org/10.1155/2014/653732 |