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Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway
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Zeitschriftentitel: | Basic & Clinical Pharmacology & Toxicology |
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Personen und Körperschaften: | , , , |
In: | Basic & Clinical Pharmacology & Toxicology, 111, 2012, 2, S. 106-112 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Wiley
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Schlagwörter: |
author_facet |
Wang, Jian Li, Yongli Wang, Xiaofeng Jiang, Chuanlu Wang, Jian Li, Yongli Wang, Xiaofeng Jiang, Chuanlu |
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author |
Wang, Jian Li, Yongli Wang, Xiaofeng Jiang, Chuanlu |
spellingShingle |
Wang, Jian Li, Yongli Wang, Xiaofeng Jiang, Chuanlu Basic & Clinical Pharmacology & Toxicology Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway Pharmacology Toxicology General Medicine |
author_sort |
wang, jian |
spelling |
Wang, Jian Li, Yongli Wang, Xiaofeng Jiang, Chuanlu 1742-7835 1742-7843 Wiley Pharmacology Toxicology General Medicine http://dx.doi.org/10.1111/j.1742-7843.2012.00870.x <jats:title>Abstract</jats:title><jats:p>New chemotherapeutic strategy should be investigated to enhance clinical management in human gliomas. Recently, ursolic acid (<jats:styled-content style="fixed-case">UA</jats:styled-content>), as a naturally occurring pentacyclic triterpene, has exhibited a potent anticancer activity in various tumour cells but remains uncertain in human glioma cells. Here, we examined whether <jats:styled-content style="fixed-case">UA</jats:styled-content> could suppress the proliferation of human glioma cell line U251, and if so, its possible molecular targets. Cell survival, apoptosis and molecular targets were identified by multiple detecting techniques, including trypan blue dye exclusion assay, electron microscopy, <jats:styled-content style="fixed-case">AO</jats:styled-content>/<jats:styled-content style="fixed-case">EB</jats:styled-content> staining, Real‐time <jats:styled-content style="fixed-case">PCR</jats:styled-content> and immunoblotting in U251 cells. The results showed that 5–20 μM of <jats:styled-content style="fixed-case">UA</jats:styled-content> suppressed proliferation and induced apoptosis of U251 cells in dose‐ and time‐dependent manners. <jats:styled-content style="fixed-case">UA</jats:styled-content> increased the activation of caspase‐3 and markedly suppressed levels of micro<jats:styled-content style="fixed-case">RNA</jats:styled-content>‐21 (miR‐21) in a time‐dependent manner. The expression of programmed cell death 4 (<jats:styled-content style="fixed-case">PDCD</jats:styled-content>4), which is a miR‐21 targeting apoptotic gene, has also been enhanced by <jats:styled-content style="fixed-case">UA</jats:styled-content>. And over‐expression of miR‐21 in U251 cells abolished the enhancement of <jats:styled-content style="fixed-case">PDCD</jats:styled-content>4 protein by <jats:styled-content style="fixed-case">UA</jats:styled-content>. More importantly, <jats:styled-content style="fixed-case">TGF</jats:styled-content>‐β1/smads signalling, as critical upstream regulators of miR‐21, has also been suppressed by <jats:styled-content style="fixed-case">UA</jats:styled-content>. These findings suggest that <jats:styled-content style="fixed-case">UA</jats:styled-content> inhibits cell growth via causing apoptosis in U251 cells by a <jats:styled-content style="fixed-case">UA</jats:styled-content>‐triggered <jats:styled-content style="fixed-case">TGF</jats:styled-content>‐β1/miR‐21/<jats:styled-content style="fixed-case">PDCD</jats:styled-content>4 pathway. This study provides an evidence for testing <jats:styled-content style="fixed-case">UA</jats:styled-content> efficacy <jats:italic>in vivo</jats:italic> and warranting future investigations examining the clinical potential of <jats:styled-content style="fixed-case">UA</jats:styled-content> in human gliomas.</jats:p> Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing <scp>TGF</scp>‐β1/miR‐21/<scp>PDCD</scp>4 Pathway Basic & Clinical Pharmacology & Toxicology |
doi_str_mv |
10.1111/j.1742-7843.2012.00870.x |
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Online Free |
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Chemie und Pharmazie |
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imprint |
Wiley, 2012 |
imprint_str_mv |
Wiley, 2012 |
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1742-7835 1742-7843 |
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2012 |
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Wiley |
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Basic & Clinical Pharmacology & Toxicology |
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title |
Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway |
title_unstemmed |
Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway |
title_full |
Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway |
title_fullStr |
Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway |
title_full_unstemmed |
Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway |
title_short |
Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway |
title_sort |
ursolic acid inhibits proliferation and induces apoptosis in human glioblastoma cell lines u251 by suppressing <scp>tgf</scp>‐β1/mir‐21/<scp>pdcd</scp>4 pathway |
topic |
Pharmacology Toxicology General Medicine |
url |
http://dx.doi.org/10.1111/j.1742-7843.2012.00870.x |
publishDate |
2012 |
physical |
106-112 |
description |
<jats:title>Abstract</jats:title><jats:p>New chemotherapeutic strategy should be investigated to enhance clinical management in human gliomas. Recently, ursolic acid (<jats:styled-content style="fixed-case">UA</jats:styled-content>), as a naturally occurring pentacyclic triterpene, has exhibited a potent anticancer activity in various tumour cells but remains uncertain in human glioma cells. Here, we examined whether <jats:styled-content style="fixed-case">UA</jats:styled-content> could suppress the proliferation of human glioma cell line U251, and if so, its possible molecular targets. Cell survival, apoptosis and molecular targets were identified by multiple detecting techniques, including trypan blue dye exclusion assay, electron microscopy, <jats:styled-content style="fixed-case">AO</jats:styled-content>/<jats:styled-content style="fixed-case">EB</jats:styled-content> staining, Real‐time <jats:styled-content style="fixed-case">PCR</jats:styled-content> and immunoblotting in U251 cells. The results showed that 5–20 μM of <jats:styled-content style="fixed-case">UA</jats:styled-content> suppressed proliferation and induced apoptosis of U251 cells in dose‐ and time‐dependent manners. <jats:styled-content style="fixed-case">UA</jats:styled-content> increased the activation of caspase‐3 and markedly suppressed levels of micro<jats:styled-content style="fixed-case">RNA</jats:styled-content>‐21 (miR‐21) in a time‐dependent manner. The expression of programmed cell death 4 (<jats:styled-content style="fixed-case">PDCD</jats:styled-content>4), which is a miR‐21 targeting apoptotic gene, has also been enhanced by <jats:styled-content style="fixed-case">UA</jats:styled-content>. And over‐expression of miR‐21 in U251 cells abolished the enhancement of <jats:styled-content style="fixed-case">PDCD</jats:styled-content>4 protein by <jats:styled-content style="fixed-case">UA</jats:styled-content>. More importantly, <jats:styled-content style="fixed-case">TGF</jats:styled-content>‐β1/smads signalling, as critical upstream regulators of miR‐21, has also been suppressed by <jats:styled-content style="fixed-case">UA</jats:styled-content>. These findings suggest that <jats:styled-content style="fixed-case">UA</jats:styled-content> inhibits cell growth via causing apoptosis in U251 cells by a <jats:styled-content style="fixed-case">UA</jats:styled-content>‐triggered <jats:styled-content style="fixed-case">TGF</jats:styled-content>‐β1/miR‐21/<jats:styled-content style="fixed-case">PDCD</jats:styled-content>4 pathway. This study provides an evidence for testing <jats:styled-content style="fixed-case">UA</jats:styled-content> efficacy <jats:italic>in vivo</jats:italic> and warranting future investigations examining the clinical potential of <jats:styled-content style="fixed-case">UA</jats:styled-content> in human gliomas.</jats:p> |
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author | Wang, Jian, Li, Yongli, Wang, Xiaofeng, Jiang, Chuanlu |
author_facet | Wang, Jian, Li, Yongli, Wang, Xiaofeng, Jiang, Chuanlu, Wang, Jian, Li, Yongli, Wang, Xiaofeng, Jiang, Chuanlu |
author_sort | wang, jian |
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description | <jats:title>Abstract</jats:title><jats:p>New chemotherapeutic strategy should be investigated to enhance clinical management in human gliomas. Recently, ursolic acid (<jats:styled-content style="fixed-case">UA</jats:styled-content>), as a naturally occurring pentacyclic triterpene, has exhibited a potent anticancer activity in various tumour cells but remains uncertain in human glioma cells. Here, we examined whether <jats:styled-content style="fixed-case">UA</jats:styled-content> could suppress the proliferation of human glioma cell line U251, and if so, its possible molecular targets. Cell survival, apoptosis and molecular targets were identified by multiple detecting techniques, including trypan blue dye exclusion assay, electron microscopy, <jats:styled-content style="fixed-case">AO</jats:styled-content>/<jats:styled-content style="fixed-case">EB</jats:styled-content> staining, Real‐time <jats:styled-content style="fixed-case">PCR</jats:styled-content> and immunoblotting in U251 cells. The results showed that 5–20 μM of <jats:styled-content style="fixed-case">UA</jats:styled-content> suppressed proliferation and induced apoptosis of U251 cells in dose‐ and time‐dependent manners. <jats:styled-content style="fixed-case">UA</jats:styled-content> increased the activation of caspase‐3 and markedly suppressed levels of micro<jats:styled-content style="fixed-case">RNA</jats:styled-content>‐21 (miR‐21) in a time‐dependent manner. The expression of programmed cell death 4 (<jats:styled-content style="fixed-case">PDCD</jats:styled-content>4), which is a miR‐21 targeting apoptotic gene, has also been enhanced by <jats:styled-content style="fixed-case">UA</jats:styled-content>. And over‐expression of miR‐21 in U251 cells abolished the enhancement of <jats:styled-content style="fixed-case">PDCD</jats:styled-content>4 protein by <jats:styled-content style="fixed-case">UA</jats:styled-content>. More importantly, <jats:styled-content style="fixed-case">TGF</jats:styled-content>‐β1/smads signalling, as critical upstream regulators of miR‐21, has also been suppressed by <jats:styled-content style="fixed-case">UA</jats:styled-content>. These findings suggest that <jats:styled-content style="fixed-case">UA</jats:styled-content> inhibits cell growth via causing apoptosis in U251 cells by a <jats:styled-content style="fixed-case">UA</jats:styled-content>‐triggered <jats:styled-content style="fixed-case">TGF</jats:styled-content>‐β1/miR‐21/<jats:styled-content style="fixed-case">PDCD</jats:styled-content>4 pathway. This study provides an evidence for testing <jats:styled-content style="fixed-case">UA</jats:styled-content> efficacy <jats:italic>in vivo</jats:italic> and warranting future investigations examining the clinical potential of <jats:styled-content style="fixed-case">UA</jats:styled-content> in human gliomas.</jats:p> |
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spelling | Wang, Jian Li, Yongli Wang, Xiaofeng Jiang, Chuanlu 1742-7835 1742-7843 Wiley Pharmacology Toxicology General Medicine http://dx.doi.org/10.1111/j.1742-7843.2012.00870.x <jats:title>Abstract</jats:title><jats:p>New chemotherapeutic strategy should be investigated to enhance clinical management in human gliomas. Recently, ursolic acid (<jats:styled-content style="fixed-case">UA</jats:styled-content>), as a naturally occurring pentacyclic triterpene, has exhibited a potent anticancer activity in various tumour cells but remains uncertain in human glioma cells. Here, we examined whether <jats:styled-content style="fixed-case">UA</jats:styled-content> could suppress the proliferation of human glioma cell line U251, and if so, its possible molecular targets. Cell survival, apoptosis and molecular targets were identified by multiple detecting techniques, including trypan blue dye exclusion assay, electron microscopy, <jats:styled-content style="fixed-case">AO</jats:styled-content>/<jats:styled-content style="fixed-case">EB</jats:styled-content> staining, Real‐time <jats:styled-content style="fixed-case">PCR</jats:styled-content> and immunoblotting in U251 cells. The results showed that 5–20 μM of <jats:styled-content style="fixed-case">UA</jats:styled-content> suppressed proliferation and induced apoptosis of U251 cells in dose‐ and time‐dependent manners. <jats:styled-content style="fixed-case">UA</jats:styled-content> increased the activation of caspase‐3 and markedly suppressed levels of micro<jats:styled-content style="fixed-case">RNA</jats:styled-content>‐21 (miR‐21) in a time‐dependent manner. The expression of programmed cell death 4 (<jats:styled-content style="fixed-case">PDCD</jats:styled-content>4), which is a miR‐21 targeting apoptotic gene, has also been enhanced by <jats:styled-content style="fixed-case">UA</jats:styled-content>. And over‐expression of miR‐21 in U251 cells abolished the enhancement of <jats:styled-content style="fixed-case">PDCD</jats:styled-content>4 protein by <jats:styled-content style="fixed-case">UA</jats:styled-content>. More importantly, <jats:styled-content style="fixed-case">TGF</jats:styled-content>‐β1/smads signalling, as critical upstream regulators of miR‐21, has also been suppressed by <jats:styled-content style="fixed-case">UA</jats:styled-content>. These findings suggest that <jats:styled-content style="fixed-case">UA</jats:styled-content> inhibits cell growth via causing apoptosis in U251 cells by a <jats:styled-content style="fixed-case">UA</jats:styled-content>‐triggered <jats:styled-content style="fixed-case">TGF</jats:styled-content>‐β1/miR‐21/<jats:styled-content style="fixed-case">PDCD</jats:styled-content>4 pathway. This study provides an evidence for testing <jats:styled-content style="fixed-case">UA</jats:styled-content> efficacy <jats:italic>in vivo</jats:italic> and warranting future investigations examining the clinical potential of <jats:styled-content style="fixed-case">UA</jats:styled-content> in human gliomas.</jats:p> Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing <scp>TGF</scp>‐β1/miR‐21/<scp>PDCD</scp>4 Pathway Basic & Clinical Pharmacology & Toxicology |
spellingShingle | Wang, Jian, Li, Yongli, Wang, Xiaofeng, Jiang, Chuanlu, Basic & Clinical Pharmacology & Toxicology, Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway, Pharmacology, Toxicology, General Medicine |
title | Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway |
title_full | Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway |
title_fullStr | Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway |
title_full_unstemmed | Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway |
title_short | Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway |
title_sort | ursolic acid inhibits proliferation and induces apoptosis in human glioblastoma cell lines u251 by suppressing <scp>tgf</scp>‐β1/mir‐21/<scp>pdcd</scp>4 pathway |
title_unstemmed | Ursolic Acid Inhibits Proliferation and Induces Apoptosis in Human Glioblastoma Cell Lines U251 by Suppressing TGF‐β1/miR‐21/PDCD4 Pathway |
topic | Pharmacology, Toxicology, General Medicine |
url | http://dx.doi.org/10.1111/j.1742-7843.2012.00870.x |