Meg3 Induces EMT and Invasion of Glioma Cells via Autophagy
Identifieur interne : 000F63 ( Ncbi/Merge ); précédent : 000F62; suivant : 000F64Meg3 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
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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>
</sec>
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<article-id pub-id-type="publisher-id">239648</article-id>
<article-id pub-id-type="doi">10.2147/OTT.S239648</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Original Research</subject>
</subj-group>
</article-categories>
<title-group><article-title>Meg3 Induces EMT and Invasion of Glioma Cells via Autophagy</article-title>
<alt-title alt-title-type="running-authors">Yang et al</alt-title>
<alt-title alt-title-type="running-title">Yang et al</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author" equal-contrib="yes"><name><surname>Yang</surname>
<given-names>Zhihao</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
<xref ref-type="aff" rid="AFF0002">2</xref>
<xref ref-type="author-notes" rid="FT0001"></xref>
</contrib>
<contrib contrib-type="author" equal-contrib="yes"><name><surname>Bian</surname>
<given-names>Erbao</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
<xref ref-type="aff" rid="AFF0002">2</xref>
<xref ref-type="author-notes" rid="FT0001"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Xu</surname>
<given-names>Yadi</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ji</surname>
<given-names>Xinghu</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tang</surname>
<given-names>Feng</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ma</surname>
<given-names>Chunchun</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Wang</surname>
<given-names>Hongliang</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zhao</surname>
<given-names>Bing</given-names>
</name>
<xref ref-type="corresp" rid="AN0001"></xref>
<xref ref-type="aff" rid="AFF0001">1</xref>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<aff id="AFF0001"><label>1</label>
<institution>Department of Neurosurgery, The Second Affiliated Hospital of Anhui Medical University</institution>
,<addr-line>Hefei</addr-line>
<addr-line>230601</addr-line>
,<country>People’s Republic of China</country>
</aff>
<aff id="AFF0002"><label>2</label>
<institution>Cerebral Vascular Disease Research Center, Anhui Medical University</institution>
,<addr-line>Hefei</addr-line>
<addr-line>230601</addr-line>
,<country>People’s Republic of China</country>
</aff>
</contrib-group>
<author-notes><corresp id="AN0001">Correspondence: Bing Zhao <institution>Department of Neurosurgery, The Second Affiliated Hospital of Anhui Medical University</institution>
, <addr-line>678 Fu Rong Road</addr-line>
, <addr-line>Hefei</addr-line>
, <addr-line>Anhui Province</addr-line>
<addr-line>230601</addr-line>
, <country>People’s Republic of China</country>
<phone>Tel +86 551 63869502</phone>
<fax>Fax +86 551 63869400</fax>
Email aydzhb@126.com</corresp>
<fn id="FT0001"><label>*</label>
<p>These authors contributed equally to this work</p>
</fn>
</author-notes>
<pub-date pub-type="epub"><day>31</day>
<month>1</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="collection"><year>2020</year>
</pub-date>
<volume>13</volume>
<fpage>989</fpage>
<lpage>1000</lpage>
<history><date date-type="received"><day>22</day>
<month>11</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>08</day>
<month>1</month>
<year>2020</year>
</date>
</history>
<permissions><copyright-statement>© 2020 Yang et al.</copyright-statement>
<copyright-year>2020</copyright-year>
<copyright-holder>Yang et al.</copyright-holder>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/3.0/"><license-p>This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at <ext-link ext-link-type="uri" xlink:href="https://www.dovepress.com/terms.php">https://www.dovepress.com/terms.php</ext-link>
and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc/3.0/">http://creativecommons.org/licenses/by-nc/3.0/</ext-link>
). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (<ext-link ext-link-type="uri" xlink:href="https://www.dovepress.com/terms.php">https://www.dovepress.com/terms.php</ext-link>
).</license-p>
</license>
</permissions>
<abstract><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>
</sec>
</abstract>
<kwd-group kwd-group-type="author"><title>Keywords</title>
<kwd>long non-coding RNA</kwd>
<kwd>Meg3</kwd>
<kwd>EMT</kwd>
<kwd>invasion</kwd>
<kwd>autophagy</kwd>
<kwd>glioma</kwd>
</kwd-group>
<funding-group><funding-statement>This project was supported by the National Natural Science Foundation of China (No. 81972348), Key Research and Development Plan Project of Anhui Province (No. 1804h08020270), College Excellent Youth Talent Support Program in Anhui Province (No. gxypZD2019019), Key Projects of Natural Science Research in Anhui Province (KJ2019A0267), Academic Funding Project for Top Talents in Colleges and Universities in Anhui Province (No. gxbjZD10), Nova Pew Plan of the Second Affiliated Hospital of Anhui Medical University (No. 2017KA01), and Anhui Medical University School Foundation (No. 2018xkj037).</funding-statement>
</funding-group>
<counts><fig-count count="6"></fig-count>
<ref-count count="56"></ref-count>
<page-count count="12"></page-count>
</counts>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
</list>
<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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