ChloroquineV1, Ncbi, Merge, bibRecord, 000496

Autophagy inhibition potentiates the anti-angiogenic property of multikinase inhibitor anlotinib through JAK2/STAT3/VEGFA signaling in non-small cell lung cancer cells.

Identifieur interne : 000496 ( Ncbi/Merge ); précédent : 000495; suivant : 000497

Autophagy inhibition potentiates the anti-angiogenic property of multikinase inhibitor anlotinib through JAK2/STAT3/VEGFA signaling in non-small cell lung cancer cells.

Source :

Journal of experimental & clinical cancer research : CR [ 1756-9966 ] ; 2019.

RBID : pubmed:30755242

Descripteurs français

KwdFr :
- Animaux, Autophagie (), Carcinome pulmonaire non à petites cellules (anatomopathologie), Carcinome pulmonaire non à petites cellules (génétique), Carcinome pulmonaire non à petites cellules (traitement médicamenteux), Facteur de croissance endothéliale vasculaire de type A (génétique), Humains, Indoles (pharmacologie), Indoles (usage thérapeutique), Kinase Janus-2 (génétique), Lignée cellulaire tumorale, Modèles animaux de maladie humaine, Prolifération cellulaire, Quinoléines (pharmacologie), Quinoléines (usage thérapeutique), Souris, Souris nude, Tests d'activité antitumorale sur modèle de xénogreffe, Transduction du signal, Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (génétique), Tumeurs du poumon (traitement médicamenteux).
MESH :
- anatomopathologie : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- génétique : Carcinome pulmonaire non à petites cellules, Facteur de croissance endothéliale vasculaire de type A, Kinase Janus-2, Tumeurs du poumon.
- pharmacologie : Indoles, Quinoléines.
- traitement médicamenteux : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- usage thérapeutique : Indoles, Quinoléines.
- Animaux, Autophagie, Humains, Lignée cellulaire tumorale, Modèles animaux de maladie humaine, Prolifération cellulaire, Souris, Souris nude, Tests d'activité antitumorale sur modèle de xénogreffe, Transduction du signal.

English descriptors

KwdEn :
- Animals, Autophagy (drug effects), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (genetics), Carcinoma, Non-Small-Cell Lung (pathology), Cell Line, Tumor, Cell Proliferation, Disease Models, Animal, Humans, Indoles (pharmacology), Indoles (therapeutic use), Janus Kinase 2 (genetics), Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (pathology), Mice, Mice, Nude, Quinolines (pharmacology), Quinolines (therapeutic use), Signal Transduction, Vascular Endothelial Growth Factor A (genetics), Xenograft Model Antitumor Assays.
MESH :
- chemical , genetics : Janus Kinase 2, Vascular Endothelial Growth Factor A.
- chemical , pharmacology : Indoles, Quinolines.
- drug effects : Autophagy.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- genetics : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- chemical , therapeutic use : Indoles, Quinolines.
- Animals, Cell Line, Tumor, Cell Proliferation, Disease Models, Animal, Humans, Mice, Mice, Nude, Signal Transduction, Xenograft Model Antitumor Assays.

Abstract

The efficacy and safety of multikinase inhibitor anlotinib have been confirmed in the treatment of advanced non-small cell lung cancer (NSCLC). However, the direct functional mechanisms of tumor lethality mediated by anlotinib were not fully elucidated, and the underlying mechanisms related to resistance remain largely elusive.

DOI: 10.1186/s13046-019-1093-3
PubMed: 30755242

Links toward previous steps (curation, corpus...)

to stream PubMed, to step Corpus: 000066
to stream PubMed, to step Curation: 000066
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pubmed:30755242

Le document en format XML

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<author><name sortKey="Jiang, Xiaodong" sort="Jiang, Xiaodong" uniqKey="Jiang X" first="Xiaodong" last="Jiang">Xiaodong Jiang</name>
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<term>Autophagy (drug effects)</term>
<term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term>
<term>Carcinoma, Non-Small-Cell Lung (genetics)</term>
<term>Carcinoma, Non-Small-Cell Lung (pathology)</term>
<term>Cell Line, Tumor</term>
<term>Cell Proliferation</term>
<term>Disease Models, Animal</term>
<term>Humans</term>
<term>Indoles (pharmacology)</term>
<term>Indoles (therapeutic use)</term>
<term>Janus Kinase 2 (genetics)</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Lung Neoplasms (genetics)</term>
<term>Lung Neoplasms (pathology)</term>
<term>Mice</term>
<term>Mice, Nude</term>
<term>Quinolines (pharmacology)</term>
<term>Quinolines (therapeutic use)</term>
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<term>Carcinome pulmonaire non à petites cellules (anatomopathologie)</term>
<term>Carcinome pulmonaire non à petites cellules (génétique)</term>
<term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term>
<term>Facteur de croissance endothéliale vasculaire de type A (génétique)</term>
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<term>Indoles (pharmacologie)</term>
<term>Indoles (usage thérapeutique)</term>
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<term>Quinoléines (usage thérapeutique)</term>
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<term>Souris nude</term>
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<front><div type="abstract" xml:lang="en">The efficacy and safety of multikinase inhibitor anlotinib have been confirmed in the treatment of advanced non-small cell lung cancer (NSCLC). However, the direct functional mechanisms of tumor lethality mediated by anlotinib were not fully elucidated, and the underlying mechanisms related to resistance remain largely elusive.</div>
</front>
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<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30755242</PMID>
<DateCompleted><Year>2019</Year>
<Month>06</Month>
<Day>24</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>02</Month>
<Day>25</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1756-9966</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>38</Volume>
<Issue>1</Issue>
<PubDate><Year>2019</Year>
<Month>Feb</Month>
<Day>12</Day>
</PubDate>
</JournalIssue>
<Title>Journal of experimental & clinical cancer research : CR</Title>
<ISOAbbreviation>J. Exp. Clin. Cancer Res.</ISOAbbreviation>
</Journal>
<ArticleTitle>Autophagy inhibition potentiates the anti-angiogenic property of multikinase inhibitor anlotinib through JAK2/STAT3/VEGFA signaling in non-small cell lung cancer cells.</ArticleTitle>
<Pagination><MedlinePgn>71</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1186/s13046-019-1093-3</ELocationID>
<Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">The efficacy and safety of multikinase inhibitor anlotinib have been confirmed in the treatment of advanced non-small cell lung cancer (NSCLC). However, the direct functional mechanisms of tumor lethality mediated by anlotinib were not fully elucidated, and the underlying mechanisms related to resistance remain largely elusive.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">Cell viability, colony formation, apoptosis and tumor growth assays were performed to examine the effect of anlotinib on lung cancer cells in vitro and in vivo. The punctate patterns of LC3-I/II were detected by confocal microscopy. HUVECs motility was detected using Transwell and scratch wound-healing assay. To visualize the microvessels, tubular formation assay was performed. The expression of LC3-I/II and beclin-1 and the changes of JAK2/STAT3/VEGFA pathway were detected by western blotting. The VEGFA levels in tumor supernatant were measured by ELISA.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Anlotinib treatment decreased cell viability and induced apoptosis in Calu-1 and A549 cells. Moreover, anlotinib induced human lung cancer cell autophagy in a dose- and time-dependent manner. Blocking autophagy enhanced the cytotoxicity and anti-angiogenic ability of anlotinib as evidenced by HUVECs migration, invasion, and tubular formation assay. Co-administration of anlotinib and chloroquine (CQ) further reduced VEGFA level in the tumor supernatant, compared with that of anlotinib or CQ treatment alone. When autophagy was induced by rapamycin, the JAK2/STAT3 pathway was activated and VEGFA was elevated, which was attenuated after deactivating STAT3 by S3I-201. Further in vivo studies showed that anlotinib inhibited tumor growth, induced autophagy and suppressed JAK2/STAT3/VEGFA pathway, and CQ enhanced this effect.</AbstractText>
<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Anlotinib induced apoptosis and protective autophagy in human lung cancer cell lines. Autophagy inhibition further enhanced the cytotoxic effects of anlotinib, and potentiated the anti-angiogenic property of anlotinib through JAK2/STAT3/VEGFA signaling.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liang</LastName>
<ForeName>Lijun</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, 222000, Jiangsu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hui</LastName>
<ForeName>Kaiyuan</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, 222000, Jiangsu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hu</LastName>
<ForeName>Chenxi</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, 222000, Jiangsu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wen</LastName>
<ForeName>Yixuan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, 222000, Jiangsu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yang</LastName>
<ForeName>Shikun</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Hepatobiliary/Liver Transplantation Center, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Key Laboratory on Living Donor Liver Transplantation of National Health and Family Planning Commission of China, Nanjing, 210029, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhu</LastName>
<ForeName>Panrong</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, 222000, Jiangsu, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Radiology 3, General Hospital of Xuzhou Coal Mining Group, the Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221002, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Lei</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, 222000, Jiangsu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xia</LastName>
<ForeName>Youyou</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, 222000, Jiangsu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Qiao</LastName>
<ForeName>Yun</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, 222000, Jiangsu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sun</LastName>
<ForeName>Wen</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, 222000, Jiangsu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fei</LastName>
<ForeName>Jiayan</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, 222000, Jiangsu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Ting</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, 222000, Jiangsu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhao</LastName>
<ForeName>Fenghua</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, 222000, Jiangsu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yang</LastName>
<ForeName>Baocheng</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Jiangsu Provincial Institute of Health Emergency, Xuzhou Medical University, Xuzhou, 221002, Jiangsu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jiang</LastName>
<ForeName>Xiaodong</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, 222000, Jiangsu, China. jxdpaper@163.com.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>81472792</GrantID>
<Agency>National Natural Science Foundation of China</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>SJCX18_0707</GrantID>
<Agency>Postgraduate Research & Practice Innovation Program of Jiangsu Province</Agency>
<Country></Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2019</Year>
<Month>02</Month>
<Day>12</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>J Exp Clin Cancer Res</MedlineTA>
<NlmUniqueID>8308647</NlmUniqueID>
<ISSNLinking>0392-9078</ISSNLinking>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D007211">Indoles</NameOfSubstance>
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<NameOfSubstance UI="C467484">VEGFA protein, human</NameOfSubstance>
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<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
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<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008819" MajorTopicYN="N">Mice, Nude</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011804" MajorTopicYN="N">Quinolines</DescriptorName>
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<Keyword MajorTopicYN="N">Anti-angiogenesis</Keyword>
<Keyword MajorTopicYN="N">Apoptosis</Keyword>
<Keyword MajorTopicYN="N">Autophagy</Keyword>
<Keyword MajorTopicYN="N">NSCLC</Keyword>
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<ArticleIdList><ArticleId IdType="pubmed">30555244</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Liang, Lijun" sort="Liang, Lijun" uniqKey="Liang L" first="Lijun" last="Liang">Lijun Liang</name>
</noRegion>
<name sortKey="Chen, Ting" sort="Chen, Ting" uniqKey="Chen T" first="Ting" last="Chen">Ting Chen</name>
<name sortKey="Fei, Jiayan" sort="Fei, Jiayan" uniqKey="Fei J" first="Jiayan" last="Fei">Jiayan Fei</name>
<name sortKey="Hu, Chenxi" sort="Hu, Chenxi" uniqKey="Hu C" first="Chenxi" last="Hu">Chenxi Hu</name>
<name sortKey="Hui, Kaiyuan" sort="Hui, Kaiyuan" uniqKey="Hui K" first="Kaiyuan" last="Hui">Kaiyuan Hui</name>
<name sortKey="Jiang, Xiaodong" sort="Jiang, Xiaodong" uniqKey="Jiang X" first="Xiaodong" last="Jiang">Xiaodong Jiang</name>
<name sortKey="Qiao, Yun" sort="Qiao, Yun" uniqKey="Qiao Y" first="Yun" last="Qiao">Yun Qiao</name>
<name sortKey="Sun, Wen" sort="Sun, Wen" uniqKey="Sun W" first="Wen" last="Sun">Wen Sun</name>
<name sortKey="Wang, Lei" sort="Wang, Lei" uniqKey="Wang L" first="Lei" last="Wang">Lei Wang</name>
<name sortKey="Wen, Yixuan" sort="Wen, Yixuan" uniqKey="Wen Y" first="Yixuan" last="Wen">Yixuan Wen</name>
<name sortKey="Xia, Youyou" sort="Xia, Youyou" uniqKey="Xia Y" first="Youyou" last="Xia">Youyou Xia</name>
<name sortKey="Yang, Baocheng" sort="Yang, Baocheng" uniqKey="Yang B" first="Baocheng" last="Yang">Baocheng Yang</name>
<name sortKey="Yang, Shikun" sort="Yang, Shikun" uniqKey="Yang S" first="Shikun" last="Yang">Shikun Yang</name>
<name sortKey="Zhao, Fenghua" sort="Zhao, Fenghua" uniqKey="Zhao F" first="Fenghua" last="Zhao">Fenghua Zhao</name>
<name sortKey="Zhu, Panrong" sort="Zhu, Panrong" uniqKey="Zhu P" first="Panrong" last="Zhu">Panrong Zhu</name>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/Ncbi/Merge

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000496 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/Ncbi/Merge/biblio.hfd -nk 000496 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Sante
   |area=    ChloroquineV1
   |flux=    Ncbi
   |étape=   Merge
   |type=    RBID
   |clé=     pubmed:30755242
   |texte=   Autophagy inhibition potentiates the anti-angiogenic property of multikinase inhibitor anlotinib through JAK2/STAT3/VEGFA signaling in non-small cell lung cancer cells.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Ncbi/Merge/RBID.i   -Sk "pubmed:30755242" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Ncbi/Merge/biblio.hfd   \
       | NlmPubMed2Wicri -a ChloroquineV1

This area was generated with Dilib version V0.6.33.
Data generation: Wed Mar 25 22:43:59 2020. Site generation: Sun Jan 31 12:44:45 2021

	Serveur d'exploration Chloroquine
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration Chloroquine

Autophagy inhibition potentiates the anti-angiogenic property of multikinase inhibitor anlotinib through JAK2/STAT3/VEGFA signaling in non-small cell lung cancer cells.

Autophagy inhibition potentiates the anti-angiogenic property of multikinase inhibitor anlotinib through JAK2/STAT3/VEGFA signaling in non-small cell lung cancer cells.

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Pour mettre un lien sur cette page dans le réseau Wicri

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