miR- 26a Sensitizes Melanoma Cells To Dabrafenib Via Targeting HMGB1-Dependent Autophagy Pathways
Identifieur interne : 000C34 ( Ncbi/Merge ); précédent : 000C33; suivant : 000C35miR- 26a Sensitizes Melanoma Cells To Dabrafenib Via Targeting HMGB1-Dependent Autophagy Pathways
Auteurs : Yan Yu [République populaire de Chine] ; Niu Xiang [République populaire de Chine] ; Min Lin [République populaire de Chine] ; Jin-Wen Huang [République populaire de Chine] ; Jing Zhang [République populaire de Chine] ; Bo Cheng [République populaire de Chine] ; Chao Ji [République populaire de Chine]Source :
- Drug Design, Development and Therapy [ 1177-8881 ] ; 2019.
Abstract
Melanoma is known as the most aggressive and lethal type of cutaneous cancer due to its rapid development of drug resistance to chemotherapy drugs.
In our study, we conducted a variety of studies, including quantitative PCR, Western blot, and autophagy and apoptosis assays to investigate the involvement of miR-26a and HMGB1 in modulation of dabrafenib sensitivity in human melanoma cell lines.
Our studies revealed that the expressions of miR-26a and HMGB1 were altered in two melanoma cell lines after dabrafenib treatment. Additionally, dabrafenib caused autophagy in melanoma and this autophagic process was regulated by miR-26a via modifying HMGB1 expression. Furthermore, silencing HMGB1-inhibited autophagy induced by dabrafenib in melanoma cells. Last, we verified that treatment with a miR-26a mimic and HMGB1 shRNA could increase the efficacy of dabrafenib in melanoma cells.
Taken together, we showed that miR-26a is involved in the regulation of dabrafenib efficacy via a HMGB1-dependent autophagy pathway in melanoma cells. These results shed light on a novel treatment for conventional dabrafenib-based chemotherapy for melanoma.
Url:
DOI: 10.2147/DDDT.S225671
PubMed: 31754297
PubMed Central: 6825511
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PMC:6825511Le document en format XML
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<front><div type="abstract" xml:lang="en"><sec id="S2001"><title>Background</title>
<p>Melanoma is known as the most aggressive and lethal type of cutaneous cancer due to its rapid development of drug resistance to chemotherapy drugs.</p>
</sec>
<sec id="S2002"><title>Methods</title>
<p>In our study, we conducted a variety of studies, including quantitative PCR, Western blot, and autophagy and apoptosis assays to investigate the involvement of miR-26a and HMGB1 in modulation of dabrafenib sensitivity in human melanoma cell lines.</p>
</sec>
<sec id="S2003"><title>Results</title>
<p>Our studies revealed that the expressions of miR-26a and HMGB1 were altered in two melanoma cell lines after dabrafenib treatment. Additionally, dabrafenib caused autophagy in melanoma and this autophagic process was regulated by miR-26a via modifying HMGB1 expression. Furthermore, silencing HMGB1-inhibited autophagy induced by dabrafenib in melanoma cells. Last, we verified that treatment with a miR-26a mimic and HMGB1 shRNA could increase the efficacy of dabrafenib in melanoma cells.</p>
</sec>
<sec id="S2004"><title>Conclusion</title>
<p>Taken together, we showed that miR-26a is involved in the regulation of dabrafenib efficacy via a HMGB1-dependent autophagy pathway in melanoma cells. These results shed light on a novel treatment for conventional dabrafenib-based chemotherapy for melanoma.</p>
</sec>
</div>
</front>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Drug Des Devel Ther</journal-id>
<journal-id journal-id-type="iso-abbrev">Drug Des Devel Ther</journal-id>
<journal-id journal-id-type="publisher-id">DDDT</journal-id>
<journal-id journal-id-type="pmc">dddt</journal-id>
<journal-title-group><journal-title>Drug Design, Development and Therapy</journal-title>
</journal-title-group>
<issn pub-type="epub">1177-8881</issn>
<publisher><publisher-name>Dove</publisher-name>
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<article-id pub-id-type="publisher-id">225671</article-id>
<article-id pub-id-type="doi">10.2147/DDDT.S225671</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Original Research</subject>
</subj-group>
</article-categories>
<title-group><article-title>miR- 26a Sensitizes Melanoma Cells To Dabrafenib Via Targeting HMGB1-Dependent Autophagy Pathways</article-title>
<alt-title alt-title-type="running-authors">Yu et al</alt-title>
<alt-title alt-title-type="running-title">Yu et al</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author" equal-contrib="yes"><name><surname>Yu</surname>
<given-names>Yan</given-names>
</name>
<xref ref-type="aff" rid="AFF0001">1</xref>
<xref ref-type="author-notes" rid="FT0001"></xref>
</contrib>
<contrib contrib-type="author" equal-contrib="yes"><name><surname>Xiang</surname>
<given-names>Niu</given-names>
</name>
<xref ref-type="aff" rid="AFF0002">2</xref>
<xref ref-type="author-notes" rid="FT0001"></xref>
</contrib>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0002-8992-6621</contrib-id>
<name><surname>Lin</surname>
<given-names>Min</given-names>
</name>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Huang</surname>
<given-names>Jin-Wen</given-names>
</name>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zhang</surname>
<given-names>Jing</given-names>
</name>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Cheng</surname>
<given-names>Bo</given-names>
</name>
<xref ref-type="corresp" rid="AN0002"></xref>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ji</surname>
<given-names>Chao</given-names>
</name>
<xref ref-type="corresp" rid="AN0001"></xref>
<xref ref-type="aff" rid="AFF0002">2</xref>
</contrib>
<aff id="AFF0001"><label>1</label>
<institution>Department of Dermatology, First Hospital of Jilin University</institution>
,<addr-line>Changchun</addr-line>
,<addr-line>Jilin</addr-line>
<addr-line>130021</addr-line>
,<country>People’s Republic of China</country>
</aff>
<aff id="AFF0002"><label>2</label>
<institution>Department of Dermatology, The First Affiliated Hospital of Fujian Medical University</institution>
,<addr-line>Fuzhou</addr-line>
,<addr-line>Fujian</addr-line>
<addr-line>350005</addr-line>
,<country>People’s Republic of China</country>
</aff>
</contrib-group>
<author-notes><corresp id="AN0001">Correspondence: Chao Ji <institution>Department of Dermatology, The First Affiliated Hospital of Fujian Medical University</institution>
, <addr-line>Fuzhou</addr-line>
, <addr-line>Fujian</addr-line>
<addr-line>350005</addr-line>
, <country>People’s Republic of China</country>
Email surpassing.ji@gmail.com</corresp>
<corresp id="AN0002">Bo Cheng <institution>Department of Dermatology, The First Affiliated Hospital of Fujian Medical University</institution>
, <addr-line>Fuzhou</addr-line>
, <addr-line>Fujian</addr-line>
<addr-line>350005</addr-line>
, <country>People’s Republic of China</country>
Email chengbo_fjmu1@163.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>29</day>
<month>10</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection"><year>2019</year>
</pub-date>
<volume>13</volume>
<fpage>3717</fpage>
<lpage>3726</lpage>
<history><date date-type="received"><day>01</day>
<month>8</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>02</day>
<month>10</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>© 2019 Yu et al.</copyright-statement>
<copyright-year>2019</copyright-year>
<copyright-holder>Yu 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>Melanoma is known as the most aggressive and lethal type of cutaneous cancer due to its rapid development of drug resistance to chemotherapy drugs.</p>
</sec>
<sec id="S2002"><title>Methods</title>
<p>In our study, we conducted a variety of studies, including quantitative PCR, Western blot, and autophagy and apoptosis assays to investigate the involvement of miR-26a and HMGB1 in modulation of dabrafenib sensitivity in human melanoma cell lines.</p>
</sec>
<sec id="S2003"><title>Results</title>
<p>Our studies revealed that the expressions of miR-26a and HMGB1 were altered in two melanoma cell lines after dabrafenib treatment. Additionally, dabrafenib caused autophagy in melanoma and this autophagic process was regulated by miR-26a via modifying HMGB1 expression. Furthermore, silencing HMGB1-inhibited autophagy induced by dabrafenib in melanoma cells. Last, we verified that treatment with a miR-26a mimic and HMGB1 shRNA could increase the efficacy of dabrafenib in melanoma cells.</p>
</sec>
<sec id="S2004"><title>Conclusion</title>
<p>Taken together, we showed that miR-26a is involved in the regulation of dabrafenib efficacy via a HMGB1-dependent autophagy pathway in melanoma cells. These results shed light on a novel treatment for conventional dabrafenib-based chemotherapy for melanoma.</p>
</sec>
</abstract>
<kwd-group kwd-group-type="author"><title>Keywords</title>
<kwd>melanoma</kwd>
<kwd>miR-26a</kwd>
<kwd>HMGB1</kwd>
<kwd>dabrafenib</kwd>
<kwd>autophagy</kwd>
<kwd>apoptosis</kwd>
</kwd-group>
<counts><fig-count count="6"></fig-count>
<ref-count count="44"></ref-count>
<page-count count="10"></page-count>
</counts>
</article-meta>
</front>
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<name sortKey="Ji, Chao" sort="Ji, Chao" uniqKey="Ji C" first="Chao" last="Ji">Chao Ji</name>
<name sortKey="Lin, Min" sort="Lin, Min" uniqKey="Lin M" first="Min" last="Lin">Min Lin</name>
<name sortKey="Xiang, Niu" sort="Xiang, Niu" uniqKey="Xiang N" first="Niu" last="Xiang">Niu Xiang</name>
<name sortKey="Zhang, Jing" sort="Zhang, Jing" uniqKey="Zhang J" first="Jing" last="Zhang">Jing Zhang</name>
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</tree>
</affiliations>
</record>
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