Suppression of Autophagy Enhanced Growth Inhibition and Apoptosis of Interferon-β in Human Glioma Cells
Identifieur interne : 001162 ( Main/Exploration ); précédent : 001161; suivant : 001163Suppression of Autophagy Enhanced Growth Inhibition and Apoptosis of Interferon-β in Human Glioma Cells
Auteurs : Yubin Li [République populaire de Chine] ; Haiyan Zhu [République populaire de Chine] ; Xian Zeng [République populaire de Chine] ; Jiajun Fan [République populaire de Chine] ; Xiaolu Qian [République populaire de Chine] ; Shaofei Wang [République populaire de Chine] ; Ziyu Wang [République populaire de Chine] ; Yun Sun [République populaire de Chine] ; Xiaodan Wang [République populaire de Chine] ; Weiwu Wang [République populaire de Chine] ; Dianwen Ju [République populaire de Chine]Source :
- Molecular Neurobiology [ 0893-7648 ] ; 2013-06-01.
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Abstract
Abstract: Interferon-beta (IFN-β) is a cytokine with anti-viral, anti-proliferative, and immunomodulatory effects. In this study, we investigated the effects of IFN-β on the induction of autophagy and the relationships among autophagy, growth inhibition, and apoptosis induced by IFN-β in human glioma cells. We found that IFN-β induced autophagosome formation and conversion of microtubule associated protein 1 light chain 3 (LC3) protein, whereas it inhibited cell growth through caspase-dependent cell apoptosis. The Akt/mTOR signaling pathway was involved in autophagy induced by IFN-β. A dose- and time-dependent increase of p-ERK 1/2 expression was also observed in human glioma cells treated with IFN-β. Autophagy induced by IFN-β was suppressed when p-ERK1/2 was impaired by treatment with U0126. We also demonstrated that suppression of autophagy significantly enhanced growth inhibition and cell apoptosis induced by IFN-β, whereas inhibition of caspase-dependent cell apoptosis impaired autophagy induced by IFN-β. Collectively, these findings indicated that autophagy induced by IFN-β was associated with the Akt/mTOR and ERK 1/2 signaling pathways, and inhibition of autophagy could enhance the growth inhibitory effects of IFN-β and increase apoptosis in human glioma cells. Together, these findings support the possibility that autophagy inhibitors may improve IFN-β therapy for gliomas.
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DOI: 10.1007/s12035-013-8403-0
Affiliations:
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Chine</country></affiliation></author></analytic><monogr></monogr><series><title level="j">Molecular Neurobiology</title><title level="j" type="abbrev">Mol Neurobiol</title><idno type="ISSN">0893-7648</idno><idno type="eISSN">1559-1182</idno><imprint><publisher>Humana Press Inc</publisher><pubPlace>New York</pubPlace><date type="published" when="2013-06-01">2013-06-01</date><biblScope unit="volume">47</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="1000">1000</biblScope><biblScope unit="page" to="1010">1010</biblScope></imprint><idno type="ISSN">0893-7648</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0893-7648</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Glioma cells</term><term>Growth inhibition</term><term>IFN-β</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Interferon-beta (IFN-β) is a cytokine with anti-viral, anti-proliferative, and immunomodulatory effects. In this study, we investigated the effects of IFN-β on the induction of autophagy and the relationships among autophagy, growth inhibition, and apoptosis induced by IFN-β in human glioma cells. We found that IFN-β induced autophagosome formation and conversion of microtubule associated protein 1 light chain 3 (LC3) protein, whereas it inhibited cell growth through caspase-dependent cell apoptosis. The Akt/mTOR signaling pathway was involved in autophagy induced by IFN-β. A dose- and time-dependent increase of p-ERK 1/2 expression was also observed in human glioma cells treated with IFN-β. Autophagy induced by IFN-β was suppressed when p-ERK1/2 was impaired by treatment with U0126. We also demonstrated that suppression of autophagy significantly enhanced growth inhibition and cell apoptosis induced by IFN-β, whereas inhibition of caspase-dependent cell apoptosis impaired autophagy induced by IFN-β. Collectively, these findings indicated that autophagy induced by IFN-β was associated with the Akt/mTOR and ERK 1/2 signaling pathways, and inhibition of autophagy could enhance the growth inhibitory effects of IFN-β and increase apoptosis in human glioma cells. Together, these findings support the possibility that autophagy inhibitors may improve IFN-β therapy for gliomas.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Li, Yubin" sort="Li, Yubin" uniqKey="Li Y" first="Yubin" last="Li">Yubin Li</name></noRegion><name sortKey="Fan, Jiajun" sort="Fan, Jiajun" uniqKey="Fan J" first="Jiajun" last="Fan">Jiajun Fan</name><name sortKey="Ju, Dianwen" sort="Ju, Dianwen" uniqKey="Ju D" first="Dianwen" last="Ju">Dianwen Ju</name><name sortKey="Ju, Dianwen" sort="Ju, Dianwen" uniqKey="Ju D" first="Dianwen" last="Ju">Dianwen Ju</name><name sortKey="Ju, Dianwen" sort="Ju, Dianwen" uniqKey="Ju D" first="Dianwen" last="Ju">Dianwen Ju</name><name sortKey="Li, Yubin" sort="Li, Yubin" uniqKey="Li Y" first="Yubin" last="Li">Yubin Li</name><name sortKey="Qian, Xiaolu" sort="Qian, Xiaolu" uniqKey="Qian X" first="Xiaolu" last="Qian">Xiaolu Qian</name><name sortKey="Sun, Yun" sort="Sun, Yun" uniqKey="Sun Y" first="Yun" last="Sun">Yun Sun</name><name sortKey="Wang, Shaofei" sort="Wang, Shaofei" uniqKey="Wang S" first="Shaofei" last="Wang">Shaofei Wang</name><name sortKey="Wang, Weiwu" sort="Wang, Weiwu" uniqKey="Wang W" first="Weiwu" last="Wang">Weiwu Wang</name><name sortKey="Wang, Xiaodan" sort="Wang, Xiaodan" uniqKey="Wang X" first="Xiaodan" last="Wang">Xiaodan Wang</name><name sortKey="Wang, Ziyu" sort="Wang, Ziyu" uniqKey="Wang Z" first="Ziyu" last="Wang">Ziyu Wang</name><name sortKey="Zeng, Xian" sort="Zeng, Xian" uniqKey="Zeng X" first="Xian" last="Zeng">Xian Zeng</name><name sortKey="Zhu, Haiyan" sort="Zhu, Haiyan" uniqKey="Zhu H" first="Haiyan" last="Zhu">Haiyan Zhu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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