Celastrol mediates autophagy and apoptosis via the ROS/JNK and Akt/mTOR signaling pathways in glioma cells
Identifieur interne : 000967 ( Main/Exploration ); précédent : 000966; suivant : 000968Celastrol mediates autophagy and apoptosis via the ROS/JNK and Akt/mTOR signaling pathways in glioma cells
Auteurs : Xihong Liu [République populaire de Chine] ; Peiyuan Zhao ; Xiujuan Wang [République populaire de Chine] ; Lei Wang [République populaire de Chine] ; Yingjun Zhu [République populaire de Chine] ; Yadi Song [République populaire de Chine] ; Wei Gao [République populaire de Chine]Source :
- Journal of Experimental & Clinical Cancer Research : CR [ 0392-9078 ] ; 2019.
Abstract
Celastrol, a triterpene compound derived from the traditional Chinese medicine
Glioma cells, including the U251, U87-MG and C6 cell lines and an animal model were used. The effects of celastrol on cells were evaluated by flow cytometry, confocal microscopy, reactive oxygen species production assay and immunoblotting after treatment of celastrol. Fisher’s exact test, a one-way ANOVA and the Mann-Whitney U-test were used to compare differences between groups. All data were analyzed using SPSS version 21.0 software.
Here, we found that exposure to celastrol induced G2/M phase arrest and apoptosis. Celastrol increased the formation of autophagosomes, accumulation of LC3B and the expression of p62 protein. Celastrol-treated glioma cells exhibited decreased cell viability after the use of autophagy inhibitors. Additionally, autophagy and apoptosis caused by celastrol in glioma cells inhibited each other. Furthermore, celastrol induced JNK activation and ROS production and inhibited the activities of Akt and mTOR kinases. JNK and ROS inhibitors significantly attenuated celastrol-trigged apoptosis and autophagy, while Akt and mTOR inhibitors had opposite effects.
In conclusion, our study revealed that celastrol caused G2/M phase arrest and trigged apoptosis and autophagy by activating ROS/JNK signaling and blocking the Akt/mTOR signaling pathway.
The online version of this article (10.1186/s13046-019-1173-4) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1186/s13046-019-1173-4
PubMed: 31053160
PubMed Central: 6500040
Affiliations:
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0004 0369 153X</institution-id><institution-id institution-id-type="GRID">grid.24696.3f</institution-id><institution>School of Traditional Chinese Medicine,</institution><institution>Capital Medical University,</institution></institution-wrap>Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0369 153X</institution-id><institution-id institution-id-type="GRID">grid.24696.3f</institution-id><institution>Beijing Key Lab of TCM Collateral Disease Theory Research,</institution><institution>Capital Medical University,</institution></institution-wrap>Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation></author><author><name sortKey="Song, Yadi" sort="Song, Yadi" uniqKey="Song Y" first="Yadi" last="Song">Yadi Song</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0369 153X</institution-id><institution-id institution-id-type="GRID">grid.24696.3f</institution-id><institution>School of Traditional Chinese Medicine,</institution><institution>Capital Medical University,</institution></institution-wrap>Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0369 153X</institution-id><institution-id institution-id-type="GRID">grid.24696.3f</institution-id><institution>Beijing Key Lab of TCM Collateral Disease Theory Research,</institution><institution>Capital Medical University,</institution></institution-wrap>Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</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-wrap><institution-id institution-id-type="ISNI">0000 0004 0369 153X</institution-id><institution-id institution-id-type="GRID">grid.24696.3f</institution-id><institution>School of Traditional Chinese Medicine,</institution><institution>Capital Medical University,</institution></institution-wrap>Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0369 153X</institution-id><institution-id institution-id-type="GRID">grid.24696.3f</institution-id><institution>Beijing Key Lab of TCM Collateral Disease Theory Research,</institution><institution>Capital Medical University,</institution></institution-wrap>Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0369 153X</institution-id><institution-id institution-id-type="GRID">grid.24696.3f</institution-id><institution>Advanced Innovation Center for Human Brain Protection,</institution><institution>Capital Medical University,</institution></institution-wrap>Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation></author></analytic><series><title level="j">Journal of Experimental & Clinical Cancer Research : CR</title><idno type="ISSN">0392-9078</idno><idno type="eISSN">1756-9966</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><title>Background</title><p id="Par1">Celastrol, a triterpene compound derived from the traditional Chinese medicine <italic>Tripterygium wilfordii</italic>, has been reported to possess potential antitumor activity towards various malignancies. However, the effect of celastrol on glioma cells and the underlying molecular mechanisms remain elusive.</p></sec><sec><title>Methods</title><p id="Par2">Glioma cells, including the U251, U87-MG and C6 cell lines and an animal model were used. The effects of celastrol on cells were evaluated by flow cytometry, confocal microscopy, reactive oxygen species production assay and immunoblotting after treatment of celastrol. Fisher’s exact test, a one-way ANOVA and the Mann-Whitney U-test were used to compare differences between groups. All data were analyzed using SPSS version 21.0 software.</p></sec><sec><title>Results</title><p id="Par3">Here, we found that exposure to celastrol induced G2/M phase arrest and apoptosis. Celastrol increased the formation of autophagosomes, accumulation of LC3B and the expression of p62 protein. Celastrol-treated glioma cells exhibited decreased cell viability after the use of autophagy inhibitors. Additionally, autophagy and apoptosis caused by celastrol in glioma cells inhibited each other. Furthermore, celastrol induced JNK activation and ROS production and inhibited the activities of Akt and mTOR kinases. JNK and ROS inhibitors significantly attenuated celastrol-trigged apoptosis and autophagy, while Akt and mTOR inhibitors had opposite effects.</p></sec><sec><title>Conclusions</title><p id="Par4">In conclusion, our study revealed that celastrol caused G2/M phase arrest and trigged apoptosis and autophagy by activating ROS/JNK signaling and blocking the Akt/mTOR signaling pathway.</p></sec><sec><title>Electronic supplementary material</title><p>The online version of this article (10.1186/s13046-019-1173-4) contains supplementary material, which is available to authorized users.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Schwartzbaum, Ja" uniqKey="Schwartzbaum J">JA Schwartzbaum</name></author><author><name sortKey="Fisher, Jl" uniqKey="Fisher J">JL Fisher</name></author><author><name sortKey="Aldape, Kd" uniqKey="Aldape K">KD Aldape</name></author><author><name sortKey="Wrensch, M" uniqKey="Wrensch M">M Wrensch</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, J" uniqKey="Liu J">J Liu</name></author><author><name sortKey="Lee, J" uniqKey="Lee J">J Lee</name></author><author><name sortKey="Salazar Hernandez, Ma" uniqKey="Salazar Hernandez M">MA Salazar Hernandez</name></author><author><name sortKey="Mazitschek, R" uniqKey="Mazitschek R">R Mazitschek</name></author><author><name sortKey="Ozcan, U" uniqKey="Ozcan U">U Ozcan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hu, M" uniqKey="Hu M">M Hu</name></author><author><name sortKey="Luo, Q" uniqKey="Luo Q">Q Luo</name></author><author><name sortKey="Alitongbieke, G" uniqKey="Alitongbieke G">G Alitongbieke</name></author><author><name sortKey="Chong, S" uniqKey="Chong S">S Chong</name></author><author><name sortKey="Xu, C" uniqKey="Xu C">C Xu</name></author><author><name sortKey="Xie, L" uniqKey="Xie L">L 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sortKey="Tsang, Yh" uniqKey="Tsang Y">YH Tsang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sun, Y" uniqKey="Sun Y">Y Sun</name></author><author><name sortKey="Huang, Yh" uniqKey="Huang Y">YH Huang</name></author><author><name sortKey="Huang, Fy" uniqKey="Huang F">FY Huang</name></author><author><name sortKey="Mei, Wl" uniqKey="Mei W">WL Mei</name></author><author><name sortKey="Liu, Q" uniqKey="Liu Q">Q Liu</name></author><author><name sortKey="Wang, Cc" uniqKey="Wang C">CC Wang</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><noCountry><name sortKey="Zhao, Peiyuan" sort="Zhao, Peiyuan" uniqKey="Zhao P" first="Peiyuan" last="Zhao">Peiyuan Zhao</name></noCountry><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="Liu, Xihong" sort="Liu, Xihong" uniqKey="Liu X" first="Xihong" last="Liu">Xihong Liu</name><name sortKey="Song, Yadi" sort="Song, Yadi" uniqKey="Song Y" first="Yadi" last="Song">Yadi Song</name><name sortKey="Song, Yadi" sort="Song, Yadi" uniqKey="Song Y" first="Yadi" last="Song">Yadi Song</name><name sortKey="Wang, Lei" sort="Wang, Lei" uniqKey="Wang L" first="Lei" last="Wang">Lei Wang</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="Wang, Xiujuan" sort="Wang, Xiujuan" uniqKey="Wang X" first="Xiujuan" last="Wang">Xiujuan Wang</name><name sortKey="Zhu, Yingjun" sort="Zhu, Yingjun" uniqKey="Zhu Y" first="Yingjun" last="Zhu">Yingjun Zhu</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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