Triptolide Induces Glioma Cell Autophagy and Apoptosis via Upregulating the ROS/JNK and Downregulating the Akt/mTOR Signaling Pathways
Identifieur interne : 000306 ( Main/Exploration ); précédent : 000305; suivant : 000307Triptolide Induces Glioma Cell Autophagy and Apoptosis via Upregulating the ROS/JNK and Downregulating the Akt/mTOR Signaling Pathways
Auteurs : Xihong Liu [République populaire de Chine] ; Peiyuan Zhao [République populaire de Chine] ; Xiujuan Wang [République populaire de Chine] ; Lei Wang [République populaire de Chine] ; Yingjun Zhu [République populaire de Chine] ; Wei Gao [République populaire de Chine]Source :
- Frontiers in Oncology [ 2234-943X ] ; 2019.
Abstract
Apoptosis and autophagy are the two prominent forms of developmental cell death, and researches have shown that crosstalk exists between these two processes. A prior study demonstrated that triptolide inhibited the proliferation of malignant glioma cells. However, whether apoptosis and autophagy participate in the inhibitory effect of triptolide in glioma cells has not been clarified. In the present study, we demonstrated that triptolide potently inhibited the growth of glioma cells by inducing cell cycle arrest at the G2/M phase. Additionally, the treatment with triptolide induced apoptosis and autophagy in various glioma cell lines. Triptolide-induced autophagy may have tumor-supporting effects. Autophagy and apoptosis could cross-inhibit each other in glioma cells treated with triptolide. Moreover, we found that triptolide induced ROS production and JNK activation and inhibited the activity of Akt and mTOR. Finally, we demonstrated that triptolide suppressed tumor growth in an orthotopic xenograft glioma model. Collectively, these data indicated that triptolide induced G2/M phase arrest, apoptosis, and autophagy via activating the ROS/JNK and blocking the Akt/mTOR signaling pathways in glioma cells. Triptolide may be a potential anti-tumor drug targeting gliomas.
Url:
DOI: 10.3389/fonc.2019.00387
PubMed: 31157167
PubMed Central: 6528693
Affiliations:
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type="wicri:Area/Main/Exploration">000306</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Triptolide Induces Glioma Cell Autophagy and Apoptosis via Upregulating the ROS/JNK and Downregulating the Akt/mTOR Signaling Pathways</title><author><name sortKey="Liu, Xihong" sort="Liu, Xihong" uniqKey="Liu X" first="Xihong" last="Liu">Xihong Liu</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>School of Traditional Chinese Medicine, Capital Medical University</institution>,<addr-line>Beijing</addr-line>,<country>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="Zhao, Peiyuan" sort="Zhao, Peiyuan" uniqKey="Zhao P" first="Peiyuan" last="Zhao">Peiyuan Zhao</name><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Basic Discipline of Integrated Chinese and Western Medicine, Henan University of Chinese Medicine</institution>,<addr-line>Henan</addr-line>,<country>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="Wang, Xiujuan" sort="Wang, Xiujuan" uniqKey="Wang X" first="Xiujuan" last="Wang">Xiujuan Wang</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>School of Traditional Chinese Medicine, Capital Medical University</institution>,<addr-line>Beijing</addr-line>,<country>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="Wang, Lei" sort="Wang, Lei" uniqKey="Wang L" first="Lei" last="Wang">Lei Wang</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>School of Traditional Chinese Medicine, Capital Medical University</institution>,<addr-line>Beijing</addr-line>,<country>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="Zhu, Yingjun" sort="Zhu, Yingjun" uniqKey="Zhu Y" first="Yingjun" last="Zhu">Yingjun Zhu</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>School of Traditional Chinese Medicine, Capital Medical University</institution>,<addr-line>Beijing</addr-line>,<country>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="Gao, Wei" sort="Gao, Wei" uniqKey="Gao W" first="Wei" last="Gao">Wei Gao</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>School of Traditional Chinese Medicine, Capital Medical University</institution>,<addr-line>Beijing</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>School of Pharmaceutical Sciences, Capital Medical University</institution>,<addr-line>Beijing</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff4"><institution>Advanced Innovation Center for Human Brain Protection, Capital Medical University</institution>,<addr-line>Beijing</addr-line>,<country>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">Frontiers in Oncology</title><idno type="eISSN">2234-943X</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Apoptosis and autophagy are the two prominent forms of developmental cell death, and researches have shown that crosstalk exists between these two processes. A prior study demonstrated that triptolide inhibited the proliferation of malignant glioma cells. However, whether apoptosis and autophagy participate in the inhibitory effect of triptolide in glioma cells has not been clarified. In the present study, we demonstrated that triptolide potently inhibited the growth of glioma cells by inducing cell cycle arrest at the G2/M phase. Additionally, the treatment with triptolide induced apoptosis and autophagy in various glioma cell lines. Triptolide-induced autophagy may have tumor-supporting effects. Autophagy and apoptosis could cross-inhibit each other in glioma cells treated with triptolide. Moreover, we found that triptolide induced ROS production and JNK activation and inhibited the activity of Akt and mTOR. Finally, we demonstrated that triptolide suppressed tumor growth in an orthotopic xenograft glioma model. Collectively, these data indicated that triptolide induced G2/M phase arrest, apoptosis, and autophagy via activating the ROS/JNK and blocking the Akt/mTOR signaling pathways in glioma cells. Triptolide may be a potential anti-tumor drug targeting gliomas.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Wen, Py" uniqKey="Wen P">PY Wen</name></author><author><name sortKey="Reardon, Da" uniqKey="Reardon D">DA Reardon</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ghinda, Dc" uniqKey="Ghinda D">DC Ghinda</name></author><author><name sortKey="Wu, Js" uniqKey="Wu J">JS Wu</name></author><author><name sortKey="Duncan, Nw" uniqKey="Duncan N">NW Duncan</name></author><author><name sortKey="Northoff, G" uniqKey="Northoff G">G Northoff</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lapointe, S" uniqKey="Lapointe S">S Lapointe</name></author><author><name sortKey="Perry, A" uniqKey="Perry A">A Perry</name></author><author><name sortKey="Butowski, Na" uniqKey="Butowski N">NA Butowski</name></author></analytic></biblStruct><biblStruct><analytic><author><name 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V">V Helfinger</name></author><author><name sortKey="Schroder, K" uniqKey="Schroder K">K Schroder</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, L" uniqKey="Zhang L">L Zhang</name></author><author><name sortKey="Kim, Sb" uniqKey="Kim S">SB Kim</name></author><author><name sortKey="Luitel, K" uniqKey="Luitel K">K Luitel</name></author><author><name sortKey="Shay, Jw" uniqKey="Shay J">JW Shay</name></author></analytic></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="Liu, Xihong" sort="Liu, Xihong" uniqKey="Liu X" first="Xihong" last="Liu">Xihong Liu</name></noRegion><name sortKey="Gao, Wei" sort="Gao, Wei" uniqKey="Gao W" first="Wei" last="Gao">Wei Gao</name><name sortKey="Gao, Wei" sort="Gao, Wei" uniqKey="Gao W" first="Wei" last="Gao">Wei Gao</name><name sortKey="Gao, Wei" sort="Gao, Wei" uniqKey="Gao W" first="Wei" last="Gao">Wei Gao</name><name sortKey="Wang, Lei" sort="Wang, Lei" uniqKey="Wang L" first="Lei" last="Wang">Lei Wang</name><name sortKey="Wang, Xiujuan" sort="Wang, Xiujuan" uniqKey="Wang X" first="Xiujuan" last="Wang">Xiujuan Wang</name><name sortKey="Zhao, Peiyuan" sort="Zhao, Peiyuan" uniqKey="Zhao P" first="Peiyuan" last="Zhao">Peiyuan Zhao</name><name sortKey="Zhu, Yingjun" sort="Zhu, Yingjun" uniqKey="Zhu Y" first="Yingjun" last="Zhu">Yingjun Zhu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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