A novel glutaminase inhibitor-968 inhibits the migration and proliferation of non-small cell lung cancer cells by targeting EGFR/ERK signaling pathway.
Identifieur interne : 000D30 ( Main/Exploration ); précédent : 000D29; suivant : 000D31A novel glutaminase inhibitor-968 inhibits the migration and proliferation of non-small cell lung cancer cells by targeting EGFR/ERK signaling pathway.
Auteurs : Tianyu Han [République populaire de Chine] ; Meng Guo [République populaire de Chine] ; Tingting Zhang [République populaire de Chine] ; Mingxi Gan [République populaire de Chine] ; Caifeng Xie [République populaire de Chine] ; Jian-Bin Wang [République populaire de Chine]Source :
- Oncotarget [ 1949-2553 ] ; 2017.
Descripteurs français
- KwdFr :
- Antienzymes (pharmacologie), Autophagie (), Bécline-1 (métabolisme), Carcinome pulmonaire non à petites cellules (métabolisme), Cycle cellulaire (), Extracellular Signal-Regulated MAP Kinases (métabolisme), Glutaminase (antagonistes et inhibiteurs), Humains, Lignée cellulaire tumorale, Mouvement cellulaire (), Points de contrôle du cycle cellulaire (), Prolifération cellulaire (), Récepteurs ErbB (métabolisme), Transduction du signal (), Tumeurs du poumon (métabolisme).
- MESH :
- antagonistes et inhibiteurs : Glutaminase.
- métabolisme : Bécline-1, Carcinome pulmonaire non à petites cellules, Extracellular Signal-Regulated MAP Kinases, Récepteurs ErbB, Tumeurs du poumon.
- pharmacologie : Antienzymes.
- Autophagie, Cycle cellulaire, Humains, Lignée cellulaire tumorale, Mouvement cellulaire, Points de contrôle du cycle cellulaire, Prolifération cellulaire, Transduction du signal.
English descriptors
- KwdEn :
- Autophagy (drug effects), Beclin-1 (metabolism), Carcinoma, Non-Small-Cell Lung (metabolism), Cell Cycle (drug effects), Cell Cycle Checkpoints (drug effects), Cell Line, Tumor, Cell Movement (drug effects), Cell Proliferation (drug effects), Enzyme Inhibitors (pharmacology), ErbB Receptors (metabolism), Extracellular Signal-Regulated MAP Kinases (metabolism), Glutaminase (antagonists & inhibitors), Humans, Lung Neoplasms (metabolism), Signal Transduction (drug effects).
- MESH :
- chemical , antagonists & inhibitors : Glutaminase.
- chemical , metabolism : Beclin-1, ErbB Receptors, Extracellular Signal-Regulated MAP Kinases.
- drug effects : Autophagy, Cell Cycle, Cell Cycle Checkpoints, Cell Movement, Cell Proliferation, Signal Transduction.
- metabolism : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- chemical , pharmacology : Enzyme Inhibitors.
- Cell Line, Tumor, Humans.
Abstract
Metabolic reprogramming is critical for cancer cell proliferation. Glutaminolysis which provides cancer cells with bioenergetics and intermediates for macromolecular synthesis have been intensively studied in recent years. Glutaminase C (GAC) is the first and rate-limiting enzyme in glutaminolysis and plays important roles in cancer initiation and progression. We previously screened a small molecule named 968, a specific inhibitor of GAC, to block the proliferation of human breast cancer cells. In this study, we found that 968 effectively inhibited NSCLC cell proliferation and migration and arrested G0/G1 phase of cell cycle. Furthermore, we demonstrated that 968 inhibited the EGFR/ERK pathway via decreasing the expression of EGFR and phospho-ERK. Apart from this, we discovered that 968 treatment induced autophagy to protect cells against apoptosis and the combination of 968 with autophagy inhibitor Chloroquine (CQ) had synergistic effects on the growth of NSCLC cells. Thus, our study pointed out a new therapeutic strategy for NSCLC treatment by combination of 968 with CQ.
DOI: 10.18632/oncotarget.14188
PubMed: 28039459
Affiliations:
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Chine</country><wicri:regionArea>Institute of Translational Medicine, Nanchang University, Nanchang City, Jiangxi 330031</wicri:regionArea><wicri:noRegion>Jiangxi 330031</wicri:noRegion></affiliation></author><author><name sortKey="Guo, Meng" sort="Guo, Meng" uniqKey="Guo M" first="Meng" last="Guo">Meng Guo</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Translational Medicine, Nanchang University, Nanchang City, Jiangxi 330031, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Translational Medicine, Nanchang University, Nanchang City, Jiangxi 330031</wicri:regionArea><wicri:noRegion>Jiangxi 330031</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Tingting" sort="Zhang, Tingting" uniqKey="Zhang T" first="Tingting" last="Zhang">Tingting Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Research Institute of Applied Biology, Shanxi University, Taiyuan, Shanxi, 030006, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Research Institute of Applied Biology, Shanxi University, Taiyuan, Shanxi, 030006</wicri:regionArea><wicri:noRegion>030006</wicri:noRegion></affiliation></author><author><name sortKey="Gan, Mingxi" sort="Gan, Mingxi" uniqKey="Gan M" first="Mingxi" last="Gan">Mingxi Gan</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Translational Medicine, Nanchang University, Nanchang City, Jiangxi 330031, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Translational Medicine, Nanchang University, Nanchang City, Jiangxi 330031</wicri:regionArea><wicri:noRegion>Jiangxi 330031</wicri:noRegion></affiliation></author><author><name sortKey="Xie, Caifeng" sort="Xie, Caifeng" uniqKey="Xie C" first="Caifeng" last="Xie">Caifeng Xie</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Translational Medicine, Nanchang University, Nanchang City, Jiangxi 330031, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Translational Medicine, Nanchang University, Nanchang City, Jiangxi 330031</wicri:regionArea><wicri:noRegion>Jiangxi 330031</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Jian Bin" sort="Wang, Jian Bin" uniqKey="Wang J" first="Jian-Bin" last="Wang">Jian-Bin Wang</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Translational Medicine, Nanchang University, Nanchang City, Jiangxi 330031, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Translational Medicine, Nanchang University, Nanchang City, Jiangxi 330031</wicri:regionArea><wicri:noRegion>Jiangxi 330031</wicri:noRegion></affiliation></author></analytic><series><title level="j">Oncotarget</title><idno type="eISSN">1949-2553</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autophagy (drug effects)</term><term>Beclin-1 (metabolism)</term><term>Carcinoma, Non-Small-Cell Lung (metabolism)</term><term>Cell Cycle (drug effects)</term><term>Cell Cycle Checkpoints (drug effects)</term><term>Cell Line, Tumor</term><term>Cell Movement (drug effects)</term><term>Cell Proliferation (drug effects)</term><term>Enzyme Inhibitors (pharmacology)</term><term>ErbB Receptors (metabolism)</term><term>Extracellular Signal-Regulated MAP Kinases (metabolism)</term><term>Glutaminase (antagonists & inhibitors)</term><term>Humans</term><term>Lung Neoplasms (metabolism)</term><term>Signal Transduction (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antienzymes (pharmacologie)</term><term>Autophagie ()</term><term>Bécline-1 (métabolisme)</term><term>Carcinome pulmonaire non à petites cellules (métabolisme)</term><term>Cycle cellulaire ()</term><term>Extracellular Signal-Regulated MAP Kinases (métabolisme)</term><term>Glutaminase (antagonistes et inhibiteurs)</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Mouvement cellulaire ()</term><term>Points de contrôle du cycle cellulaire ()</term><term>Prolifération cellulaire ()</term><term>Récepteurs ErbB (métabolisme)</term><term>Transduction du signal ()</term><term>Tumeurs du poumon (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Glutaminase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Beclin-1</term><term>ErbB Receptors</term><term>Extracellular Signal-Regulated MAP Kinases</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Glutaminase</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term><term>Cell Cycle</term><term>Cell Cycle Checkpoints</term><term>Cell Movement</term><term>Cell Proliferation</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Bécline-1</term><term>Carcinome pulmonaire non à petites cellules</term><term>Extracellular Signal-Regulated MAP Kinases</term><term>Récepteurs ErbB</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antienzymes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Enzyme Inhibitors</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Autophagie</term><term>Cycle cellulaire</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Mouvement cellulaire</term><term>Points de contrôle du cycle cellulaire</term><term>Prolifération cellulaire</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Metabolic reprogramming is critical for cancer cell proliferation. Glutaminolysis which provides cancer cells with bioenergetics and intermediates for macromolecular synthesis have been intensively studied in recent years. Glutaminase C (GAC) is the first and rate-limiting enzyme in glutaminolysis and plays important roles in cancer initiation and progression. We previously screened a small molecule named 968, a specific inhibitor of GAC, to block the proliferation of human breast cancer cells. In this study, we found that 968 effectively inhibited NSCLC cell proliferation and migration and arrested G0/G1 phase of cell cycle. Furthermore, we demonstrated that 968 inhibited the EGFR/ERK pathway via decreasing the expression of EGFR and phospho-ERK. Apart from this, we discovered that 968 treatment induced autophagy to protect cells against apoptosis and the combination of 968 with autophagy inhibitor Chloroquine (CQ) had synergistic effects on the growth of NSCLC cells. Thus, our study pointed out a new therapeutic strategy for NSCLC treatment by combination of 968 with CQ.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Han, Tianyu" sort="Han, Tianyu" uniqKey="Han T" first="Tianyu" last="Han">Tianyu Han</name></noRegion><name sortKey="Gan, Mingxi" sort="Gan, Mingxi" uniqKey="Gan M" first="Mingxi" last="Gan">Mingxi Gan</name><name sortKey="Guo, Meng" sort="Guo, Meng" uniqKey="Guo M" first="Meng" last="Guo">Meng Guo</name><name sortKey="Wang, Jian Bin" sort="Wang, Jian Bin" uniqKey="Wang J" first="Jian-Bin" last="Wang">Jian-Bin Wang</name><name sortKey="Xie, Caifeng" sort="Xie, Caifeng" uniqKey="Xie C" first="Caifeng" last="Xie">Caifeng Xie</name><name sortKey="Zhang, Tingting" sort="Zhang, Tingting" uniqKey="Zhang T" first="Tingting" last="Zhang">Tingting Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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