miR- 26a Sensitizes Melanoma Cells To Dabrafenib Via Targeting HMGB1-Dependent Autophagy Pathways
Identifieur interne : 000259 ( Main/Exploration ); précédent : 000258; suivant : 000260miR- 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
Affiliations:
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sortKey="Xiang, Niu" sort="Xiang, Niu" uniqKey="Xiang N" first="Niu" last="Xiang">Niu Xiang</name><affiliation wicri:level="1"><nlm:aff id="AFF0002"><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></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Lin, Min" sort="Lin, Min" uniqKey="Lin M" first="Min" last="Lin">Min Lin</name><affiliation wicri:level="1"><nlm:aff id="AFF0002"><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></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Huang, Jin Wen" sort="Huang, Jin Wen" uniqKey="Huang J" first="Jin-Wen" last="Huang">Jin-Wen Huang</name><affiliation wicri:level="1"><nlm:aff id="AFF0002"><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></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Zhang, Jing" sort="Zhang, Jing" uniqKey="Zhang J" first="Jing" last="Zhang">Jing Zhang</name><affiliation wicri:level="1"><nlm:aff id="AFF0002"><institution>Department of Dermatology, The First Affiliated Hospital of Fujian Medical 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wicri:level="1"><nlm:aff id="AFF0002"><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></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></analytic><series><title level="j">Drug Design, Development and Therapy</title><idno type="eISSN">1177-8881</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><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><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Yu, Yan" sort="Yu, Yan" uniqKey="Yu Y" first="Yan" last="Yu">Yan Yu</name></noRegion><name sortKey="Cheng, Bo" sort="Cheng, Bo" uniqKey="Cheng B" first="Bo" last="Cheng">Bo Cheng</name><name sortKey="Huang, Jin Wen" sort="Huang, Jin Wen" uniqKey="Huang J" first="Jin-Wen" last="Huang">Jin-Wen Huang</name><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></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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