Apatinib-induced protective autophagy and apoptosis through the AKT-mTOR pathway in anaplastic thyroid cancer.
Identifieur interne : 000C52 ( Main/Exploration ); précédent : 000C51; suivant : 000C53Apatinib-induced protective autophagy and apoptosis through the AKT-mTOR pathway in anaplastic thyroid cancer.
Auteurs : Haoran Feng [République populaire de Chine] ; Xi Cheng [République populaire de Chine] ; Jie Kuang [République populaire de Chine] ; Lingxie Chen [République populaire de Chine] ; Stanley Yuen [États-Unis] ; Minmin Shi [République populaire de Chine] ; Juyong Liang [République populaire de Chine] ; Baiyong Shen [République populaire de Chine] ; Zhijian Jin [République populaire de Chine] ; Jiqi Yan [République populaire de Chine] ; Weihua Qiu [République populaire de Chine]Source :
- Cell death & disease [ 2041-4889 ] ; 2018.
Descripteurs français
- KwdFr :
- Animaux, Antinéoplasiques (pharmacologie), Apoptose (), Autophagie (), Carcinome anaplasique de la thyroïde (métabolisme), Carcinome anaplasique de la thyroïde (traitement médicamenteux), Chloroquine (pharmacologie), Humains, Inhibiteurs de protéines kinases (pharmacologie), Lignée cellulaire tumorale, Mâle, Prolifération cellulaire (), Protéines proto-oncogènes c-akt (métabolisme), Pyridines (pharmacologie), Souris, Souris de lignée BALB C, Souris nude, Sérine-thréonine kinases TOR (métabolisme), Transduction du signal ().
- MESH :
- métabolisme : Carcinome anaplasique de la thyroïde, Protéines proto-oncogènes c-akt, Sérine-thréonine kinases TOR.
- pharmacologie : Antinéoplasiques, Chloroquine, Inhibiteurs de protéines kinases, Pyridines.
- traitement médicamenteux : Carcinome anaplasique de la thyroïde.
- Animaux, Apoptose, Autophagie, Humains, Lignée cellulaire tumorale, Mâle, Prolifération cellulaire, Souris, Souris de lignée BALB C, Souris nude, Transduction du signal.
English descriptors
- KwdEn :
- Animals, Antineoplastic Agents (pharmacology), Apoptosis (drug effects), Autophagy (drug effects), Cell Line, Tumor, Cell Proliferation (drug effects), Chloroquine (pharmacology), Humans, Male, Mice, Mice, Inbred BALB C, Mice, Nude, Protein Kinase Inhibitors (pharmacology), Proto-Oncogene Proteins c-akt (metabolism), Pyridines (pharmacology), Signal Transduction (drug effects), TOR Serine-Threonine Kinases (metabolism), Thyroid Carcinoma, Anaplastic (drug therapy), Thyroid Carcinoma, Anaplastic (metabolism).
- MESH :
- chemical , metabolism : Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases.
- chemical , pharmacology : Antineoplastic Agents, Chloroquine, Protein Kinase Inhibitors, Pyridines.
- drug effects : Apoptosis, Autophagy, Cell Proliferation, Signal Transduction.
- drug therapy : Thyroid Carcinoma, Anaplastic.
- metabolism : Thyroid Carcinoma, Anaplastic.
- Animals, Cell Line, Tumor, Humans, Male, Mice, Mice, Inbred BALB C, Mice, Nude.
Abstract
Apatinib, an inhibitor of vascular endothelial growth factor receptor-2, has been shown to promote anti-cancer action across a wide range of malignancies, including gastric, lung, and breast cancers. Our previous study showed that apatinib increases apoptosis in anaplastic thyroid carcinoma (ATC), but the direct functional mechanism of tumor lethality mediated by apatinib is still unknown. In this study, we demonstrated that apatinib induced both autophagy and apoptosis in human ATC cells through downregulation of p-AKT and p-mTOR signals via the AKT/mTOR pathway. Moreover, inhibition of apatinib-induced autophagy increased apatinib-induced apoptosis in ATC cells, and additional tumor suppression was critically produced by the combination of apatinib and the autophagy inhibitor chloroquine in vivo and in vitro. These findings showed that both autophagy and AKT/mTOR signals were engaged in ATC cell death evoked by apatinib. ATC patients might benefit from the new anti-cancer drug, and molecular targeted treatment in combination with autophagy inhibitors shows promise as a treatment improvement.
DOI: 10.1038/s41419-018-1054-3
PubMed: 30301881
Affiliations:
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Le document en format XML
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Medicine, 200025, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Liang, Juyong" sort="Liang, Juyong" uniqKey="Liang J" first="Juyong" last="Liang">Juyong Liang</name><affiliation wicri:level="1"><nlm:affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Shen, Baiyong" sort="Shen, Baiyong" uniqKey="Shen B" 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(pharmacology)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>Pyridines (pharmacology)</term><term>Signal Transduction (drug effects)</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Thyroid Carcinoma, Anaplastic (drug therapy)</term><term>Thyroid Carcinoma, Anaplastic (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antinéoplasiques (pharmacologie)</term><term>Apoptose ()</term><term>Autophagie ()</term><term>Carcinome anaplasique de la thyroïde (métabolisme)</term><term>Carcinome anaplasique de la thyroïde (traitement médicamenteux)</term><term>Chloroquine (pharmacologie)</term><term>Humains</term><term>Inhibiteurs de protéines kinases (pharmacologie)</term><term>Lignée cellulaire tumorale</term><term>Mâle</term><term>Prolifération cellulaire ()</term><term>Protéines proto-oncogènes c-akt (métabolisme)</term><term>Pyridines (pharmacologie)</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Souris nude</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Transduction du signal ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Proto-Oncogene Proteins c-akt</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term><term>Chloroquine</term><term>Protein Kinase Inhibitors</term><term>Pyridines</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Proliferation</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Thyroid Carcinoma, Anaplastic</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Thyroid Carcinoma, Anaplastic</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Carcinome anaplasique de la thyroïde</term><term>Protéines proto-oncogènes c-akt</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques</term><term>Chloroquine</term><term>Inhibiteurs de protéines kinases</term><term>Pyridines</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Carcinome anaplasique de la thyroïde</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Humans</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Mice, Nude</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Autophagie</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Mâle</term><term>Prolifération cellulaire</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Souris nude</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Apatinib, an inhibitor of vascular endothelial growth factor receptor-2, has been shown to promote anti-cancer action across a wide range of malignancies, including gastric, lung, and breast cancers. Our previous study showed that apatinib increases apoptosis in anaplastic thyroid carcinoma (ATC), but the direct functional mechanism of tumor lethality mediated by apatinib is still unknown. In this study, we demonstrated that apatinib induced both autophagy and apoptosis in human ATC cells through downregulation of p-AKT and p-mTOR signals via the AKT/mTOR pathway. Moreover, inhibition of apatinib-induced autophagy increased apatinib-induced apoptosis in ATC cells, and additional tumor suppression was critically produced by the combination of apatinib and the autophagy inhibitor chloroquine in vivo and in vitro. These findings showed that both autophagy and AKT/mTOR signals were engaged in ATC cell death evoked by apatinib. ATC patients might benefit from the new anti-cancer drug, and molecular targeted treatment in combination with autophagy inhibitors shows promise as a treatment improvement.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Feng, Haoran" sort="Feng, Haoran" uniqKey="Feng H" first="Haoran" last="Feng">Haoran Feng</name></noRegion><name sortKey="Chen, Lingxie" sort="Chen, Lingxie" uniqKey="Chen L" first="Lingxie" last="Chen">Lingxie Chen</name><name sortKey="Cheng, Xi" sort="Cheng, Xi" uniqKey="Cheng X" first="Xi" last="Cheng">Xi Cheng</name><name sortKey="Jin, Zhijian" sort="Jin, Zhijian" uniqKey="Jin Z" first="Zhijian" last="Jin">Zhijian Jin</name><name sortKey="Kuang, Jie" sort="Kuang, Jie" uniqKey="Kuang J" first="Jie" last="Kuang">Jie Kuang</name><name sortKey="Liang, Juyong" sort="Liang, Juyong" uniqKey="Liang J" first="Juyong" last="Liang">Juyong Liang</name><name sortKey="Qiu, Weihua" sort="Qiu, Weihua" uniqKey="Qiu W" first="Weihua" last="Qiu">Weihua Qiu</name><name sortKey="Shen, Baiyong" sort="Shen, Baiyong" uniqKey="Shen B" first="Baiyong" last="Shen">Baiyong Shen</name><name sortKey="Shi, Minmin" sort="Shi, Minmin" uniqKey="Shi M" first="Minmin" last="Shi">Minmin Shi</name><name sortKey="Yan, Jiqi" sort="Yan, Jiqi" uniqKey="Yan J" first="Jiqi" last="Yan">Jiqi Yan</name></country><country name="États-Unis"><region name="État de New York"><name sortKey="Yuen, Stanley" sort="Yuen, Stanley" uniqKey="Yuen S" first="Stanley" last="Yuen">Stanley Yuen</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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