ChloroquineV1, Main, Exploration, bibRecord, 000F02

Autophagy facilitates lung adenocarcinoma resistance to cisplatin treatment by activation of AMPK/mTOR signaling pathway.

Identifieur interne : 000F02 ( Main/Exploration ); précédent : 000F01; suivant : 000F03

Autophagy facilitates lung adenocarcinoma resistance to cisplatin treatment by activation of AMPK/mTOR signaling pathway.

Auteurs : Tao Wu [République populaire de Chine] ; Min-Cong Wang [République populaire de Chine] ; Li Jing [République populaire de Chine] ; Zhi-Yan Liu [République populaire de Chine] ; Hui Guo [République populaire de Chine] ; Ying Liu [République populaire de Chine] ; Yi-Yang Bai [République populaire de Chine] ; Yang-Zi Cheng [République populaire de Chine] ; Ke-Jun Nan [République populaire de Chine] ; Xuan Liang [République populaire de Chine]

Source :

Drug design, development and therapy [ 1177-8881 ] ; 2015.

RBID : pubmed:26715839

Descripteurs français

English descriptors

KwdEn :
- AMP-Activated Protein Kinases (metabolism), Adenocarcinoma (drug therapy), Adenocarcinoma (metabolism), Adenocarcinoma (pathology), Adenocarcinoma of Lung, Antineoplastic Agents (chemistry), Antineoplastic Agents (pharmacology), Autophagy (drug effects), Cell Proliferation (drug effects), Cell Survival (drug effects), Cisplatin (chemistry), Cisplatin (pharmacology), Dose-Response Relationship, Drug, Drug Resistance, Neoplasm (drug effects), Drug Screening Assays, Antitumor, Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (metabolism), Lung Neoplasms (pathology), Signal Transduction (drug effects), Structure-Activity Relationship, TOR Serine-Threonine Kinases (metabolism), Tumor Cells, Cultured.
MESH :
- chemical , chemistry : Antineoplastic Agents, Cisplatin.
- chemical , metabolism : AMP-Activated Protein Kinases, TOR Serine-Threonine Kinases.
- drug effects : Autophagy, Cell Proliferation, Cell Survival, Drug Resistance, Neoplasm, Signal Transduction.
- drug therapy : Adenocarcinoma, Lung Neoplasms.
- metabolism : Adenocarcinoma, Lung Neoplasms.
- pathology : Adenocarcinoma, Lung Neoplasms.
- chemical , pharmacology : Antineoplastic Agents, Cisplatin.
- Adenocarcinoma of Lung, Dose-Response Relationship, Drug, Drug Screening Assays, Antitumor, Humans, Structure-Activity Relationship, Tumor Cells, Cultured.

Abstract

Resistance to cisplatin-based therapy is a major challenge in the control of lung cancer progression. However, the underlying mechanisms remain largely unclear. Autophagy is closely associated with resistance to lung cancer therapy, but the function of autophagy in cisplatin treatment is still controversial. Here, we investigated whether autophagy was involved in lung adenocarcinoma resistance to cisplatin and further elucidated the underlying molecular mechanisms. Cisplatin-refractory lung adenocarcinoma cells increased autophagic vacuole formation detected by monodansylcadaverine staining. When exposed to cisplatin, lung adeno-carcinoma cells demonstrated increased levels of autophagy detected by MAP1A/1B LC3B and mammalian homologue of yeast Atg6 (Beclin-1) expression using Western blot analysis. Activation of cisplatin-induced autophagic flux was increased by using chloroquine (CQ), which can accumulate LC3B-II protein and increase punctate distribution of LC3B localization. The combination of cisplatin with CQ was more potent than cisplatin alone in inhibiting lung adenocarcinoma cell growth, which also increased cisplatin-induced apoptosis. Compared to cisplatin treatment alone, the combination of cisplatin and CQ decreased p-AMPK and increased p-mTOR protein expressions, in addition, the AMPK inhibitor Compound C plus cisplatin downregulated p-AMPK and upregulated p-mTOR as well as depressed LC3B cleavage. These findings demonstrate that activation of autophagy is a hallmark of cisplatin exposure in human lung adenocarcinoma cells, and that there is a cisplatin-induced autophagic response via activation of the AMPK/mTOR signaling pathway. We speculate that autophagy can be used as a novel therapeutic target to overcome cisplatin-resistant lung adenocarcinoma.

DOI: 10.2147/DDDT.S95606
PubMed: 26715839

Affiliations:

République populaire de Chine

Le document en format XML

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<term>Adenocarcinoma (drug therapy)</term>
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<term>Adenocarcinoma (pathology)</term>
<term>Adenocarcinoma of Lung</term>
<term>Antineoplastic Agents (chemistry)</term>
<term>Antineoplastic Agents (pharmacology)</term>
<term>Autophagy (drug effects)</term>
<term>Cell Proliferation (drug effects)</term>
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<term>Cisplatin (pharmacology)</term>
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<term>Drug Resistance, Neoplasm (drug effects)</term>
<term>Drug Screening Assays, Antitumor</term>
<term>Humans</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Lung Neoplasms (metabolism)</term>
<term>Lung Neoplasms (pathology)</term>
<term>Signal Transduction (drug effects)</term>
<term>Structure-Activity Relationship</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
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</keywords>
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<term>Adénocarcinome (anatomopathologie)</term>
<term>Adénocarcinome (métabolisme)</term>
<term>Adénocarcinome (traitement médicamenteux)</term>
<term>Antinéoplasiques ()</term>
<term>Antinéoplasiques (pharmacologie)</term>
<term>Autophagie ()</term>
<term>Cellules cancéreuses en culture</term>
<term>Cisplatine ()</term>
<term>Cisplatine (pharmacologie)</term>
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<term>Prolifération cellulaire ()</term>
<term>Relation dose-effet des médicaments</term>
<term>Relation structure-activité</term>
<term>Résistance aux médicaments antinéoplasiques ()</term>
<term>Survie cellulaire ()</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Tests de criblage d'agents antitumoraux</term>
<term>Transduction du signal ()</term>
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<term>TOR Serine-Threonine Kinases</term>
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<term>Tumeurs du poumon</term>
</keywords>
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<term>Cell Proliferation</term>
<term>Cell Survival</term>
<term>Drug Resistance, Neoplasm</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Adenocarcinoma</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Adenocarcinoma</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>AMP-Activated Protein Kinases</term>
<term>Adénocarcinome</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Adenocarcinoma</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques</term>
<term>Cisplatine</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term>
<term>Cisplatin</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Adénocarcinome</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adenocarcinoma of Lung</term>
<term>Dose-Response Relationship, Drug</term>
<term>Drug Screening Assays, Antitumor</term>
<term>Humans</term>
<term>Structure-Activity Relationship</term>
<term>Tumor Cells, Cultured</term>
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<term>Autophagie</term>
<term>Cellules cancéreuses en culture</term>
<term>Cisplatine</term>
<term>Humains</term>
<term>Prolifération cellulaire</term>
<term>Relation dose-effet des médicaments</term>
<term>Relation structure-activité</term>
<term>Résistance aux médicaments antinéoplasiques</term>
<term>Survie cellulaire</term>
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<front><div type="abstract" xml:lang="en">Resistance to cisplatin-based therapy is a major challenge in the control of lung cancer progression. However, the underlying mechanisms remain largely unclear. Autophagy is closely associated with resistance to lung cancer therapy, but the function of autophagy in cisplatin treatment is still controversial. Here, we investigated whether autophagy was involved in lung adenocarcinoma resistance to cisplatin and further elucidated the underlying molecular mechanisms. Cisplatin-refractory lung adenocarcinoma cells increased autophagic vacuole formation detected by monodansylcadaverine staining. When exposed to cisplatin, lung adeno-carcinoma cells demonstrated increased levels of autophagy detected by MAP1A/1B LC3B and mammalian homologue of yeast Atg6 (Beclin-1) expression using Western blot analysis. Activation of cisplatin-induced autophagic flux was increased by using chloroquine (CQ), which can accumulate LC3B-II protein and increase punctate distribution of LC3B localization. The combination of cisplatin with CQ was more potent than cisplatin alone in inhibiting lung adenocarcinoma cell growth, which also increased cisplatin-induced apoptosis. Compared to cisplatin treatment alone, the combination of cisplatin and CQ decreased p-AMPK and increased p-mTOR protein expressions, in addition, the AMPK inhibitor Compound C plus cisplatin downregulated p-AMPK and upregulated p-mTOR as well as depressed LC3B cleavage. These findings demonstrate that activation of autophagy is a hallmark of cisplatin exposure in human lung adenocarcinoma cells, and that there is a cisplatin-induced autophagic response via activation of the AMPK/mTOR signaling pathway. We speculate that autophagy can be used as a novel therapeutic target to overcome cisplatin-resistant lung adenocarcinoma. </div>
</front>
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<name sortKey="Cheng, Yang Zi" sort="Cheng, Yang Zi" uniqKey="Cheng Y" first="Yang-Zi" last="Cheng">Yang-Zi Cheng</name>
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<name sortKey="Liu, Ying" sort="Liu, Ying" uniqKey="Liu Y" first="Ying" last="Liu">Ying Liu</name>
<name sortKey="Liu, Zhi Yan" sort="Liu, Zhi Yan" uniqKey="Liu Z" first="Zhi-Yan" last="Liu">Zhi-Yan Liu</name>
<name sortKey="Nan, Ke Jun" sort="Nan, Ke Jun" uniqKey="Nan K" first="Ke-Jun" last="Nan">Ke-Jun Nan</name>
<name sortKey="Wang, Min Cong" sort="Wang, Min Cong" uniqKey="Wang M" first="Min-Cong" last="Wang">Min-Cong Wang</name>
</country>
</tree>
</affiliations>
</record>

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EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/Main/Exploration

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000F02 | SxmlIndent | more

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Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Sante
   |area=    ChloroquineV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:26715839
   |texte=   Autophagy facilitates lung adenocarcinoma resistance to cisplatin treatment by activation of AMPK/mTOR signaling pathway.
}}

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HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:26715839" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/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

Autophagy facilitates lung adenocarcinoma resistance to cisplatin treatment by activation of AMPK/mTOR signaling pathway.

Autophagy facilitates lung adenocarcinoma resistance to cisplatin treatment by activation of AMPK/mTOR signaling pathway.

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Pour générer des pages wiki

	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.