Apatinib-induced protective autophagy and apoptosis through the AKT-mTOR pathway in anaplastic thyroid cancer.
Identifieur interne : 000081 ( PubMed/Corpus ); précédent : 000080; suivant : 000082Apatinib-induced protective autophagy and apoptosis through the AKT-mTOR pathway in anaplastic thyroid cancer.
Auteurs : Haoran Feng ; Xi Cheng ; Jie Kuang ; Lingxie Chen ; Stanley Yuen ; Minmin Shi ; Juyong Liang ; Baiyong Shen ; Zhijian Jin ; Jiqi Yan ; Weihua QiuSource :
- Cell death & disease [ 2041-4889 ] ; 2018.
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
Links to Exploration step
pubmed:30301881Le document en format XML
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Tong University School of Medicine, 200025, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Lingxie" sort="Chen, Lingxie" uniqKey="Chen L" first="Lingxie" last="Chen">Lingxie Chen</name><affiliation><nlm:affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Yuen, Stanley" sort="Yuen, Stanley" uniqKey="Yuen S" first="Stanley" last="Yuen">Stanley Yuen</name><affiliation><nlm:affiliation>Biology Chemistry Major, University at Albany, New York, NY, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Shi, Minmin" sort="Shi, Minmin" uniqKey="Shi M" first="Minmin" last="Shi">Minmin Shi</name><affiliation><nlm:affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Liang, Juyong" sort="Liang, Juyong" uniqKey="Liang J" first="Juyong" last="Liang">Juyong Liang</name><affiliation><nlm:affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Shen, Baiyong" sort="Shen, Baiyong" uniqKey="Shen B" first="Baiyong" last="Shen">Baiyong Shen</name><affiliation><nlm:affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Jin, Zhijian" sort="Jin, Zhijian" uniqKey="Jin Z" first="Zhijian" last="Jin">Zhijian Jin</name><affiliation><nlm:affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China. drjinzj@163.com.</nlm:affiliation></affiliation></author><author><name sortKey="Yan, Jiqi" sort="Yan, Jiqi" 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General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Lingxie" sort="Chen, Lingxie" uniqKey="Chen L" first="Lingxie" last="Chen">Lingxie Chen</name><affiliation><nlm:affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Yuen, Stanley" sort="Yuen, Stanley" uniqKey="Yuen S" first="Stanley" last="Yuen">Stanley Yuen</name><affiliation><nlm:affiliation>Biology Chemistry Major, University at Albany, New York, NY, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Shi, Minmin" sort="Shi, Minmin" uniqKey="Shi M" first="Minmin" last="Shi">Minmin Shi</name><affiliation><nlm:affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Liang, Juyong" sort="Liang, Juyong" uniqKey="Liang J" first="Juyong" last="Liang">Juyong Liang</name><affiliation><nlm:affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Shen, Baiyong" sort="Shen, Baiyong" uniqKey="Shen B" first="Baiyong" last="Shen">Baiyong Shen</name><affiliation><nlm:affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</nlm:affiliation></affiliation></author><author><name sortKey="Jin, Zhijian" sort="Jin, Zhijian" uniqKey="Jin Z" first="Zhijian" last="Jin">Zhijian Jin</name><affiliation><nlm:affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China. drjinzj@163.com.</nlm:affiliation></affiliation></author><author><name sortKey="Yan, Jiqi" sort="Yan, Jiqi" uniqKey="Yan J" first="Jiqi" last="Yan">Jiqi Yan</name><affiliation><nlm:affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China. yanjiqi@aliyun.com.</nlm:affiliation></affiliation></author><author><name sortKey="Qiu, Weihua" sort="Qiu, Weihua" uniqKey="Qiu W" first="Weihua" last="Qiu">Weihua Qiu</name><affiliation><nlm:affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China. qwh11072@rjh.com.cn.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Cell death & disease</title><idno type="eISSN">2041-4889</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antineoplastic Agents (pharmacology)</term><term>Apoptosis (drug effects)</term><term>Autophagy (drug effects)</term><term>Cell Line, Tumor</term><term>Cell Proliferation (drug effects)</term><term>Chloroquine (pharmacology)</term><term>Humans</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Mice, Nude</term><term>Protein Kinase Inhibitors (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="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" 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></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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30301881</PMID><DateCompleted><Year>2019</Year><Month>11</Month><Day>13</Day></DateCompleted><DateRevised><Year>2019</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2041-4889</ISSN><JournalIssue CitedMedium="Internet"><Volume>9</Volume><Issue>10</Issue><PubDate><Year>2018</Year><Month>10</Month><Day>09</Day></PubDate></JournalIssue><Title>Cell death & disease</Title><ISOAbbreviation>Cell Death Dis</ISOAbbreviation></Journal><ArticleTitle>Apatinib-induced protective autophagy and apoptosis through the AKT-mTOR pathway in anaplastic thyroid cancer.</ArticleTitle><Pagination><MedlinePgn>1030</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41419-018-1054-3</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Feng</LastName><ForeName>Haoran</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheng</LastName><ForeName>Xi</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kuang</LastName><ForeName>Jie</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Lingxie</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yuen</LastName><ForeName>Stanley</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Biology Chemistry Major, University at Albany, New York, NY, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shi</LastName><ForeName>Minmin</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liang</LastName><ForeName>Juyong</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shen</LastName><ForeName>Baiyong</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jin</LastName><ForeName>Zhijian</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China. drjinzj@163.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China. drjinzj@163.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Jiqi</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China. yanjiqi@aliyun.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China. yanjiqi@aliyun.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Qiu</LastName><ForeName>Weihua</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China. qwh11072@rjh.com.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025, Shanghai, China. qwh11072@rjh.com.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>10</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cell Death 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