Meg3 Induces EMT and Invasion of Glioma Cells via Autophagy
Identifieur interne : 000114 ( an2020/Analysis ); précédent : 000113; suivant : 000115Meg3 Induces EMT and Invasion of Glioma Cells via Autophagy
Auteurs : Zhihao Yang [République populaire de Chine] ; Erbao Bian [République populaire de Chine] ; Yadi Xu [République populaire de Chine] ; Xinghu Ji [République populaire de Chine] ; Feng Tang [République populaire de Chine] ; Chunchun Ma [République populaire de Chine] ; Hongliang Wang [République populaire de Chine] ; Bing Zhao [République populaire de Chine]Source :
- OncoTargets and therapy [ 1178-6930 ] ; 2020.
Abstract
Glioma is one of the most common malignant tumors. Glioblastoma (grade IV) is considered the most malignant form of human brain tumors. Maternal expression gene 3 (Meg3) encodes a non-coding RNA (ncRNA) that plays an important role in the development and progression of cancer. However, the role of Meg3 in glioma cells remains largely unclear.
Reverse transcription-quantitative (RT-q) PCR was conducted to evaluate the mRNA expression related to cell autophagy and EMT while protein expression was detected by Western blotting. Staining of acidic vacuoles and immunofluorescence staining were used to detect autophagy. The ability of cells to migrate and invade was detected by Transwell migration and invasion assays.
In the present study, it was found that the overexpression of Meg3 induced EMT, migration and invasion of glioma cells, whereas Meg3 overexpression induced autophagy of glioma cells. More importantly, the inhibition of autophagy impaired the EMT of glioma cells. In addition, Meg3-induced EMT, migration and invasion could be partially reversed by autophagy inhibitors, chloroquine (CQ) and Lys05, in glioma cells.
All data suggest that Meg3 induces EMT and invasion of glioma cells via autophagy. Overall, the findings of the present study demonstrate the importance of Meg3 in the molecular etiology of glioma, which also indicate its potential applications in the treatment of glioma.
Url:
DOI: 10.2147/OTT.S239648
PubMed: 32099402
PubMed Central: 6999788
Affiliations:
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PMC:6999788Le document en format XML
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<front><div type="abstract" xml:lang="en"><sec id="S2001"><title>Background</title>
<p>Glioma is one of the most common malignant tumors. Glioblastoma (grade IV) is considered the most malignant form of human brain tumors. Maternal expression gene 3 (Meg3) encodes a non-coding RNA (ncRNA) that plays an important role in the development and progression of cancer. However, the role of Meg3 in glioma cells remains largely unclear.</p>
</sec>
<sec id="S2002"><title>Methods</title>
<p>Reverse transcription-quantitative (RT-q) PCR was conducted to evaluate the mRNA expression related to cell autophagy and EMT while protein expression was detected by Western blotting. Staining of acidic vacuoles and immunofluorescence staining were used to detect autophagy. The ability of cells to migrate and invade was detected by Transwell migration and invasion assays.</p>
</sec>
<sec id="S2003"><title>Results</title>
<p>In the present study, it was found that the overexpression of Meg3 induced EMT, migration and invasion of glioma cells, whereas Meg3 overexpression induced autophagy of glioma cells. More importantly, the inhibition of autophagy impaired the EMT of glioma cells. In addition, Meg3-induced EMT, migration and invasion could be partially reversed by autophagy inhibitors, chloroquine (CQ) and Lys05, in glioma cells.</p>
</sec>
<sec id="S2004"><title>Conclusion</title>
<p>All data suggest that Meg3 induces EMT and invasion of glioma cells via autophagy. Overall, the findings of the present study demonstrate the importance of Meg3 in the molecular etiology of glioma, which also indicate its potential applications in the treatment of glioma.</p>
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<tree><country name="République populaire de Chine"><noRegion><name sortKey="Yang, Zhihao" sort="Yang, Zhihao" uniqKey="Yang Z" first="Zhihao" last="Yang">Zhihao Yang</name>
</noRegion>
<name sortKey="Bian, Erbao" sort="Bian, Erbao" uniqKey="Bian E" first="Erbao" last="Bian">Erbao Bian</name>
<name sortKey="Bian, Erbao" sort="Bian, Erbao" uniqKey="Bian E" first="Erbao" last="Bian">Erbao Bian</name>
<name sortKey="Ji, Xinghu" sort="Ji, Xinghu" uniqKey="Ji X" first="Xinghu" last="Ji">Xinghu Ji</name>
<name sortKey="Ji, Xinghu" sort="Ji, Xinghu" uniqKey="Ji X" first="Xinghu" last="Ji">Xinghu Ji</name>
<name sortKey="Ma, Chunchun" sort="Ma, Chunchun" uniqKey="Ma C" first="Chunchun" last="Ma">Chunchun Ma</name>
<name sortKey="Ma, Chunchun" sort="Ma, Chunchun" uniqKey="Ma C" first="Chunchun" last="Ma">Chunchun Ma</name>
<name sortKey="Tang, Feng" sort="Tang, Feng" uniqKey="Tang F" first="Feng" last="Tang">Feng Tang</name>
<name sortKey="Tang, Feng" sort="Tang, Feng" uniqKey="Tang F" first="Feng" last="Tang">Feng Tang</name>
<name sortKey="Wang, Hongliang" sort="Wang, Hongliang" uniqKey="Wang H" first="Hongliang" last="Wang">Hongliang Wang</name>
<name sortKey="Wang, Hongliang" sort="Wang, Hongliang" uniqKey="Wang H" first="Hongliang" last="Wang">Hongliang Wang</name>
<name sortKey="Xu, Yadi" sort="Xu, Yadi" uniqKey="Xu Y" first="Yadi" last="Xu">Yadi Xu</name>
<name sortKey="Xu, Yadi" sort="Xu, Yadi" uniqKey="Xu Y" first="Yadi" last="Xu">Yadi Xu</name>
<name sortKey="Yang, Zhihao" sort="Yang, Zhihao" uniqKey="Yang Z" first="Zhihao" last="Yang">Zhihao Yang</name>
<name sortKey="Zhao, Bing" sort="Zhao, Bing" uniqKey="Zhao B" first="Bing" last="Zhao">Bing Zhao</name>
<name sortKey="Zhao, Bing" sort="Zhao, Bing" uniqKey="Zhao B" first="Bing" last="Zhao">Bing Zhao</name>
</country>
</tree>
</affiliations>
</record>
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