GlutaredoxinV1, Main, Exploration, bibRecord, 000169

GLRX inhibition enhances the effects of geftinib in EGFR-TKI-resistant NSCLC cells through FoxM1 signaling pathway.

Identifieur interne : 000169 ( Main/Exploration ); précédent : 000168; suivant : 000170

GLRX inhibition enhances the effects of geftinib in EGFR-TKI-resistant NSCLC cells through FoxM1 signaling pathway.

Auteurs : Linlin Wang [République populaire de Chine] ; Jing Liu [République populaire de Chine] ; Jinguo Liu [République populaire de Chine] ; Xiaoyan Chen [République populaire de Chine] ; Meijia Chang [République populaire de Chine] ; Jing Li [République populaire de Chine] ; Jian Zhou [République populaire de Chine] ; Chunxue Bai [République populaire de Chine] ; Yuanlin Song [République populaire de Chine]

Source :

Journal of cancer research and clinical oncology [ 1432-1335 ] ; 2019.

RBID : pubmed:30661098

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (genetics), Carcinoma, Non-Small-Cell Lung (metabolism), Cell Line, Tumor (MeSH), Cell Proliferation (MeSH), Drug Resistance, Neoplasm (MeSH), ErbB Receptors (antagonists & inhibitors), ErbB Receptors (genetics), ErbB Receptors (metabolism), Forkhead Box Protein M1 (metabolism), Gefitinib (pharmacology), Glutaredoxins (antagonists & inhibitors), Glutaredoxins (metabolism), Humans (MeSH), Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (metabolism), Male (MeSH), Mice (MeSH), Mice, Inbred C3H (MeSH), Mice, Nude (MeSH), NF-E2-Related Factor 2 (metabolism), Protein Kinase Inhibitors (pharmacology), Signal Transduction (MeSH), Up-Regulation (MeSH).
MESH :
- chemical , antagonists & inhibitors : ErbB Receptors, Glutaredoxins.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- genetics : Carcinoma, Non-Small-Cell Lung, ErbB Receptors, Lung Neoplasms.
- metabolism : Carcinoma, Non-Small-Cell Lung, ErbB Receptors, Forkhead Box Protein M1, Glutaredoxins, Lung Neoplasms, NF-E2-Related Factor 2.
- chemical , pharmacology : Gefitinib, Protein Kinase Inhibitors.
- Animals, Cell Line, Tumor, Cell Proliferation, Drug Resistance, Neoplasm, Humans, Male, Mice, Mice, Inbred C3H, Mice, Nude, Signal Transduction, Up-Regulation.

Abstract

PURPOSE

Non-small-cell lung cancer (NSCLC) is the most common form of lung cancer. Gefitinib is one of the most accepted therapies against NSCLC in those carrying EGFR mutations, but it is only effective in approximately 20% of patients with NSCLC. Thus, alternative therapeutic interventions are urgently needed to overcome gefitinib resistance. Glutaredoxin (GLRX) plays a key role in oxidative stress. However, whether GLRX inhibition could enhance gefitinib efficacy in the gefitinib-resistant NSCLC cells is unknown. In this study, we aimed to determine whether combined inhibition of GLRX could enhance growth-inhibitory effects of gefitinib in gefitinib-resistant NSCLC cells.

METHODS

Real-time PCR and western blotting were used to examine the mRNA and protein levels of GLRX in gefitinib-sensitive PC9 and HCC827 and -resistant human lung adenocarcinoma PC9R, HCC827R, and H1975 cells. Cell Counting Kit-8, flow cytometry, JC-1 staining, and reactive oxygen species (ROS) assays were used to evaluate cell proliferation, cell cycle progression, mitochondrial membrane potential, and ROS generation, respectively. Mouse tumor xenografts were used to assess the effect of GLRX in vivo.

RESULTS

We found that GLRX was upregulated in gefitinib-resistant PC9R, HCC827R, and H1975 cells. GLRX inhibition enhanced the effects of geftinib in gefitinib-resistant cell proliferation in vitro and in vivo and promoted apoptosis and cell cycle arrest via the EGFR/Forkhead Box M1 (FoxM1) signaling pathway, indicating that combined inhibition of GLRX could enhance growth-inhibitory effects of gefitinib in gefitinib-resistant NSCLC cells.

CONCLUSIONS

Our results suggest that GLRX inhibition enhances the effects of geftinib in EGFR-TKI-resistant NSCLC cells. Thus, GLRX may represent a therapeutic target for increasing the efficiency of gefitinib treatment.

DOI: 10.1007/s00432-019-02845-y
PubMed: 30661098

Affiliations:

République populaire de Chine

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<sourceDesc><biblStruct><analytic><title xml:lang="en">GLRX inhibition enhances the effects of geftinib in EGFR-TKI-resistant NSCLC cells through FoxM1 signaling pathway.</title>
<author><name sortKey="Wang, Linlin" sort="Wang, Linlin" uniqKey="Wang L" first="Linlin" last="Wang">Linlin Wang</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032</wicri:regionArea>
<wicri:noRegion>200032</wicri:noRegion>
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<affiliation wicri:level="1"><nlm:affiliation>Shanghai Respiratory Research Institute, Shanghai, China.</nlm:affiliation>
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<wicri:noRegion>Shanghai</wicri:noRegion>
</affiliation>
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<author><name sortKey="Chen, Xiaoyan" sort="Chen, Xiaoyan" uniqKey="Chen X" first="Xiaoyan" last="Chen">Xiaoyan Chen</name>
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<affiliation wicri:level="1"><nlm:affiliation>Shanghai Respiratory Research Institute, Shanghai, China.</nlm:affiliation>
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<author><name sortKey="Chang, Meijia" sort="Chang, Meijia" uniqKey="Chang M" first="Meijia" last="Chang">Meijia Chang</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032</wicri:regionArea>
<wicri:noRegion>200032</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Shanghai Respiratory Research Institute, Shanghai, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shanghai Respiratory Research Institute, Shanghai</wicri:regionArea>
<wicri:noRegion>Shanghai</wicri:noRegion>
</affiliation>
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<author><name sortKey="Li, Jing" sort="Li, Jing" uniqKey="Li J" first="Jing" last="Li">Jing Li</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032</wicri:regionArea>
<wicri:noRegion>200032</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Shanghai Respiratory Research Institute, Shanghai, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shanghai Respiratory Research Institute, Shanghai</wicri:regionArea>
<wicri:noRegion>Shanghai</wicri:noRegion>
</affiliation>
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<author><name sortKey="Zhou, Jian" sort="Zhou, Jian" uniqKey="Zhou J" first="Jian" last="Zhou">Jian Zhou</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China. zhou.jian@fudan.edu.cn.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032</wicri:regionArea>
<wicri:noRegion>200032</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Shanghai Respiratory Research Institute, Shanghai, China. zhou.jian@fudan.edu.cn.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shanghai Respiratory Research Institute, Shanghai</wicri:regionArea>
<wicri:noRegion>Shanghai</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Bai, Chunxue" sort="Bai, Chunxue" uniqKey="Bai C" first="Chunxue" last="Bai">Chunxue Bai</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China. bai.chunxue@zs-hospital.sh.cn.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032</wicri:regionArea>
<wicri:noRegion>200032</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:affiliation>Shanghai Respiratory Research Institute, Shanghai, China. bai.chunxue@zs-hospital.sh.cn.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Shanghai Respiratory Research Institute, Shanghai</wicri:regionArea>
<wicri:noRegion>Shanghai</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Song, Yuanlin" sort="Song, Yuanlin" uniqKey="Song Y" first="Yuanlin" last="Song">Yuanlin Song</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China. song.yuanlin@zs-hospital.sh.cn.</nlm:affiliation>
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<wicri:noRegion>200032</wicri:noRegion>
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<series><title level="j">Journal of cancer research and clinical oncology</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term>
<term>Carcinoma, Non-Small-Cell Lung (genetics)</term>
<term>Carcinoma, Non-Small-Cell Lung (metabolism)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Cell Proliferation (MeSH)</term>
<term>Drug Resistance, Neoplasm (MeSH)</term>
<term>ErbB Receptors (antagonists & inhibitors)</term>
<term>ErbB Receptors (genetics)</term>
<term>ErbB Receptors (metabolism)</term>
<term>Forkhead Box Protein M1 (metabolism)</term>
<term>Gefitinib (pharmacology)</term>
<term>Glutaredoxins (antagonists & inhibitors)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Lung Neoplasms (genetics)</term>
<term>Lung Neoplasms (metabolism)</term>
<term>Male (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C3H (MeSH)</term>
<term>Mice, Nude (MeSH)</term>
<term>NF-E2-Related Factor 2 (metabolism)</term>
<term>Protein Kinase Inhibitors (pharmacology)</term>
<term>Signal Transduction (MeSH)</term>
<term>Up-Regulation (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Carcinome pulmonaire non à petites cellules (génétique)</term>
<term>Carcinome pulmonaire non à petites cellules (métabolisme)</term>
<term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term>
<term>Facteur-2 apparenté à NF-E2 (métabolisme)</term>
<term>Glutarédoxines (antagonistes et inhibiteurs)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Géfitinib (pharmacologie)</term>
<term>Humains (MeSH)</term>
<term>Inhibiteurs de protéines kinases (pharmacologie)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Prolifération cellulaire (MeSH)</term>
<term>Protéine M1 à motif en tête de fourche (métabolisme)</term>
<term>Récepteurs ErbB (antagonistes et inhibiteurs)</term>
<term>Récepteurs ErbB (génétique)</term>
<term>Récepteurs ErbB (métabolisme)</term>
<term>Régulation positive (MeSH)</term>
<term>Résistance aux médicaments antinéoplasiques (MeSH)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C3H (MeSH)</term>
<term>Souris nude (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
<term>Tumeurs du poumon (génétique)</term>
<term>Tumeurs du poumon (métabolisme)</term>
<term>Tumeurs du poumon (traitement médicamenteux)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>ErbB Receptors</term>
<term>Glutaredoxins</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Glutarédoxines</term>
<term>Récepteurs ErbB</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term>
<term>ErbB Receptors</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term>
<term>Récepteurs ErbB</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term>
<term>ErbB Receptors</term>
<term>Forkhead Box Protein M1</term>
<term>Glutaredoxins</term>
<term>Lung Neoplasms</term>
<term>NF-E2-Related Factor 2</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term>
<term>Facteur-2 apparenté à NF-E2</term>
<term>Glutarédoxines</term>
<term>Protéine M1 à motif en tête de fourche</term>
<term>Récepteurs ErbB</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Géfitinib</term>
<term>Inhibiteurs de protéines kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Gefitinib</term>
<term>Protein Kinase Inhibitors</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line, Tumor</term>
<term>Cell Proliferation</term>
<term>Drug Resistance, Neoplasm</term>
<term>Humans</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C3H</term>
<term>Mice, Nude</term>
<term>Signal Transduction</term>
<term>Up-Regulation</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Mâle</term>
<term>Prolifération cellulaire</term>
<term>Régulation positive</term>
<term>Résistance aux médicaments antinéoplasiques</term>
<term>Souris</term>
<term>Souris de lignée C3H</term>
<term>Souris nude</term>
<term>Transduction du signal</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p><b>PURPOSE</b>
</p>
<p>Non-small-cell lung cancer (NSCLC) is the most common form of lung cancer. Gefitinib is one of the most accepted therapies against NSCLC in those carrying EGFR mutations, but it is only effective in approximately 20% of patients with NSCLC. Thus, alternative therapeutic interventions are urgently needed to overcome gefitinib resistance. Glutaredoxin (GLRX) plays a key role in oxidative stress. However, whether GLRX inhibition could enhance gefitinib efficacy in the gefitinib-resistant NSCLC cells is unknown. In this study, we aimed to determine whether combined inhibition of GLRX could enhance growth-inhibitory effects of gefitinib in gefitinib-resistant NSCLC cells.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS</b>
</p>
<p>Real-time PCR and western blotting were used to examine the mRNA and protein levels of GLRX in gefitinib-sensitive PC9 and HCC827 and -resistant human lung adenocarcinoma PC9R, HCC827R, and H1975 cells. Cell Counting Kit-8, flow cytometry, JC-1 staining, and reactive oxygen species (ROS) assays were used to evaluate cell proliferation, cell cycle progression, mitochondrial membrane potential, and ROS generation, respectively. Mouse tumor xenografts were used to assess the effect of GLRX in vivo.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>We found that GLRX was upregulated in gefitinib-resistant PC9R, HCC827R, and H1975 cells. GLRX inhibition enhanced the effects of geftinib in gefitinib-resistant cell proliferation in vitro and in vivo and promoted apoptosis and cell cycle arrest via the EGFR/Forkhead Box M1 (FoxM1) signaling pathway, indicating that combined inhibition of GLRX could enhance growth-inhibitory effects of gefitinib in gefitinib-resistant NSCLC cells.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>Our results suggest that GLRX inhibition enhances the effects of geftinib in EGFR-TKI-resistant NSCLC cells. Thus, GLRX may represent a therapeutic target for increasing the efficiency of gefitinib treatment.</p>
</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30661098</PMID>
<DateCompleted><Year>2019</Year>
<Month>04</Month>
<Day>15</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>02</Month>
<Day>25</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1432-1335</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>145</Volume>
<Issue>4</Issue>
<PubDate><Year>2019</Year>
<Month>Apr</Month>
</PubDate>
</JournalIssue>
<Title>Journal of cancer research and clinical oncology</Title>
<ISOAbbreviation>J Cancer Res Clin Oncol</ISOAbbreviation>
</Journal>
<ArticleTitle>GLRX inhibition enhances the effects of geftinib in EGFR-TKI-resistant NSCLC cells through FoxM1 signaling pathway.</ArticleTitle>
<Pagination><MedlinePgn>861-872</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1007/s00432-019-02845-y</ELocationID>
<Abstract><AbstractText Label="PURPOSE" NlmCategory="OBJECTIVE">Non-small-cell lung cancer (NSCLC) is the most common form of lung cancer. Gefitinib is one of the most accepted therapies against NSCLC in those carrying EGFR mutations, but it is only effective in approximately 20% of patients with NSCLC. Thus, alternative therapeutic interventions are urgently needed to overcome gefitinib resistance. Glutaredoxin (GLRX) plays a key role in oxidative stress. However, whether GLRX inhibition could enhance gefitinib efficacy in the gefitinib-resistant NSCLC cells is unknown. In this study, we aimed to determine whether combined inhibition of GLRX could enhance growth-inhibitory effects of gefitinib in gefitinib-resistant NSCLC cells.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">Real-time PCR and western blotting were used to examine the mRNA and protein levels of GLRX in gefitinib-sensitive PC9 and HCC827 and -resistant human lung adenocarcinoma PC9R, HCC827R, and H1975 cells. Cell Counting Kit-8, flow cytometry, JC-1 staining, and reactive oxygen species (ROS) assays were used to evaluate cell proliferation, cell cycle progression, mitochondrial membrane potential, and ROS generation, respectively. Mouse tumor xenografts were used to assess the effect of GLRX in vivo.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">We found that GLRX was upregulated in gefitinib-resistant PC9R, HCC827R, and H1975 cells. GLRX inhibition enhanced the effects of geftinib in gefitinib-resistant cell proliferation in vitro and in vivo and promoted apoptosis and cell cycle arrest via the EGFR/Forkhead Box M1 (FoxM1) signaling pathway, indicating that combined inhibition of GLRX could enhance growth-inhibitory effects of gefitinib in gefitinib-resistant NSCLC cells.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Our results suggest that GLRX inhibition enhances the effects of geftinib in EGFR-TKI-resistant NSCLC cells. Thus, GLRX may represent a therapeutic target for increasing the efficiency of gefitinib treatment.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Linlin</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Shanghai Respiratory Research Institute, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Jing</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, The Affiliated Yantai Yuhuangding Hospital, Qingdao University, Yantai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Jinguo</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Xiaoyan</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Shanghai Respiratory Research Institute, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chang</LastName>
<ForeName>Meijia</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Shanghai Respiratory Research Institute, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Jing</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Shanghai Respiratory Research Institute, Shanghai, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhou</LastName>
<ForeName>Jian</ForeName>
<Initials>J</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0003-4736-9457</Identifier>
<AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China. zhou.jian@fudan.edu.cn.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Shanghai Respiratory Research Institute, Shanghai, China. zhou.jian@fudan.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bai</LastName>
<ForeName>Chunxue</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China. bai.chunxue@zs-hospital.sh.cn.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Shanghai Respiratory Research Institute, Shanghai, China. bai.chunxue@zs-hospital.sh.cn.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Song</LastName>
<ForeName>Yuanlin</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China. song.yuanlin@zs-hospital.sh.cn.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Shanghai Respiratory Research Institute, Shanghai, China. song.yuanlin@zs-hospital.sh.cn.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>2018ZX09201002-006</GrantID>
<Agency>National Science & Technology Major Project "Key New Drug Creation and Manufacturing Program"</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>81400018, 81570028, and 81770039</GrantID>
<Agency>National Natural Science Foundation of China</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>2016ZSLC05</GrantID>
<Agency>Zhongshan Hospital Clinical Research Foundation</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>2013BAI09B00</GrantID>
<Agency>National Key Technology Research and Development Program of the Ministry of Science and Technology of China</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>2015CB553404</GrantID>
<Agency>State Key Basic Research Program (973) project</Agency>
<Country></Country>
</Grant>
<Grant><GrantID>ZR2016HL39</GrantID>
<Agency>Project of Natural Science Foundation of Shandong Province</Agency>
<Country></Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2019</Year>
<Month>01</Month>
<Day>19</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Germany</Country>
<MedlineTA>J Cancer Res Clin Oncol</MedlineTA>
<NlmUniqueID>7902060</NlmUniqueID>
<ISSNLinking>0171-5216</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C107585">FOXM1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000072278">Forkhead Box Protein M1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C516005">GLRX protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051267">NF-E2-Related Factor 2</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C495635">NFE2L2 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D047428">Protein Kinase Inhibitors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber>
<NameOfSubstance UI="C512478">EGFR protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber>
<NameOfSubstance UI="D066246">ErbB Receptors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>S65743JHBS</RegistryNumber>
<NameOfSubstance UI="D000077156">Gefitinib</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002289" MajorTopicYN="N">Carcinoma, Non-Small-Cell Lung</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019008" MajorTopicYN="N">Drug Resistance, Neoplasm</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D066246" MajorTopicYN="N">ErbB Receptors</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000072278" MajorTopicYN="N">Forkhead Box Protein M1</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000077156" MajorTopicYN="N">Gefitinib</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008809" MajorTopicYN="N">Mice, Inbred C3H</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008819" MajorTopicYN="N">Mice, Nude</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051267" MajorTopicYN="N">NF-E2-Related Factor 2</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D047428" MajorTopicYN="N">Protein Kinase Inhibitors</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Drug resistance</Keyword>
<Keyword MajorTopicYN="N">FoxM1</Keyword>
<Keyword MajorTopicYN="N">GLRX</Keyword>
<Keyword MajorTopicYN="N">Gefitinib</Keyword>
<Keyword MajorTopicYN="N">Non-small-cell lung cancer</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year>
<Month>05</Month>
<Day>28</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2019</Year>
<Month>01</Month>
<Day>11</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2019</Year>
<Month>1</Month>
<Day>21</Day>
<Hour>6</Hour>
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<Month>4</Month>
<Day>16</Day>
<Hour>6</Hour>
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<ArticleIdList><ArticleId IdType="pubmed">372193</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 1976 Jul;73(7):2275-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7783</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="Wang, Linlin" sort="Wang, Linlin" uniqKey="Wang L" first="Linlin" last="Wang">Linlin Wang</name>
</noRegion>
<name sortKey="Bai, Chunxue" sort="Bai, Chunxue" uniqKey="Bai C" first="Chunxue" last="Bai">Chunxue Bai</name>
<name sortKey="Bai, Chunxue" sort="Bai, Chunxue" uniqKey="Bai C" first="Chunxue" last="Bai">Chunxue Bai</name>
<name sortKey="Chang, Meijia" sort="Chang, Meijia" uniqKey="Chang M" first="Meijia" last="Chang">Meijia Chang</name>
<name sortKey="Chang, Meijia" sort="Chang, Meijia" uniqKey="Chang M" first="Meijia" last="Chang">Meijia Chang</name>
<name sortKey="Chen, Xiaoyan" sort="Chen, Xiaoyan" uniqKey="Chen X" first="Xiaoyan" last="Chen">Xiaoyan Chen</name>
<name sortKey="Chen, Xiaoyan" sort="Chen, Xiaoyan" uniqKey="Chen X" first="Xiaoyan" last="Chen">Xiaoyan Chen</name>
<name sortKey="Li, Jing" sort="Li, Jing" uniqKey="Li J" first="Jing" last="Li">Jing Li</name>
<name sortKey="Li, Jing" sort="Li, Jing" uniqKey="Li J" first="Jing" last="Li">Jing Li</name>
<name sortKey="Liu, Jing" sort="Liu, Jing" uniqKey="Liu J" first="Jing" last="Liu">Jing Liu</name>
<name sortKey="Liu, Jinguo" sort="Liu, Jinguo" uniqKey="Liu J" first="Jinguo" last="Liu">Jinguo Liu</name>
<name sortKey="Song, Yuanlin" sort="Song, Yuanlin" uniqKey="Song Y" first="Yuanlin" last="Song">Yuanlin Song</name>
<name sortKey="Song, Yuanlin" sort="Song, Yuanlin" uniqKey="Song Y" first="Yuanlin" last="Song">Yuanlin Song</name>
<name sortKey="Wang, Linlin" sort="Wang, Linlin" uniqKey="Wang L" first="Linlin" last="Wang">Linlin Wang</name>
<name sortKey="Zhou, Jian" sort="Zhou, Jian" uniqKey="Zhou J" first="Jian" last="Zhou">Jian Zhou</name>
<name sortKey="Zhou, Jian" sort="Zhou, Jian" uniqKey="Zhou J" first="Jian" last="Zhou">Jian Zhou</name>
</country>
</tree>
</affiliations>
</record>

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   |texte=   GLRX inhibition enhances the effects of geftinib in EGFR-TKI-resistant NSCLC cells through FoxM1 signaling pathway.
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GLRX inhibition enhances the effects of geftinib in EGFR-TKI-resistant NSCLC cells through FoxM1 signaling pathway.

GLRX inhibition enhances the effects of geftinib in EGFR-TKI-resistant NSCLC cells through FoxM1 signaling pathway.

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