Chloroquine in combination with aptamer-modified nanocomplexes for tumor vessel normalization and efficient erlotinib/Survivin shRNA co-delivery to overcome drug resistance in EGFR-mutated non-small cell lung cancer.
Identifieur interne : 000099 ( PubMed/Corpus ); précédent : 000098; suivant : 000100Chloroquine in combination with aptamer-modified nanocomplexes for tumor vessel normalization and efficient erlotinib/Survivin shRNA co-delivery to overcome drug resistance in EGFR-mutated non-small cell lung cancer.
Auteurs : Tingting Lv ; Ziying Li ; Liang Xu ; Yingying Zhang ; Haijun Chen ; Yu GaoSource :
- Acta biomaterialia [ 1878-7568 ] ; 2018.
English descriptors
- KwdEn :
- Animals, Aptamers, Nucleotide (chemistry), Aptamers, Nucleotide (pharmacokinetics), Aptamers, Nucleotide (pharmacology), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (genetics), Carcinoma, Non-Small-Cell Lung (metabolism), Carcinoma, Non-Small-Cell Lung (pathology), Cell Line, Tumor, Chloroquine (chemistry), Chloroquine (pharmacokinetics), Chloroquine (pharmacology), Drug Resistance, Neoplasm (drug effects), Drug Resistance, Neoplasm (genetics), ErbB Receptors (genetics), ErbB Receptors (metabolism), Erlotinib Hydrochloride (chemistry), Erlotinib Hydrochloride (pharmacokinetics), Erlotinib Hydrochloride (pharmacology), Female, Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (metabolism), Lung Neoplasms (pathology), Mice, Mice, Inbred BALB C, Mice, Nude, Mutation, Nanoparticles (chemistry), Nanoparticles (therapeutic use), Neoplasm Proteins (genetics), Neoplasm Proteins (metabolism), RNA, Small Interfering (chemistry), RNA, Small Interfering (pharmacokinetics), RNA, Small Interfering (pharmacology), Survivin, Xenograft Model Antitumor Assays.
- MESH :
- chemical , chemistry : Aptamers, Nucleotide, Chloroquine, Erlotinib Hydrochloride, RNA, Small Interfering.
- chemical , genetics : ErbB Receptors, Neoplasm Proteins.
- chemical , metabolism : ErbB Receptors, Neoplasm Proteins.
- chemical , pharmacokinetics : Aptamers, Nucleotide, Chloroquine, Erlotinib Hydrochloride, RNA, Small Interfering.
- chemical , pharmacology : Aptamers, Nucleotide, Chloroquine, Erlotinib Hydrochloride, RNA, Small Interfering.
- chemistry : Nanoparticles.
- drug effects : Drug Resistance, Neoplasm.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- genetics : Carcinoma, Non-Small-Cell Lung, Drug Resistance, Neoplasm, Lung Neoplasms.
- metabolism : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- therapeutic use : Nanoparticles.
- Animals, Cell Line, Tumor, Female, Humans, Mice, Mice, Inbred BALB C, Mice, Nude, Mutation, Survivin, Xenograft Model Antitumor Assays.
Abstract
Although novel molecular targeted drugs have been recognized as an effective therapy for non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) activating mutations, their efficacy fails to meet the expectation due to the acquired resistance in tumors. Up-regulation of the anti-apoptotic protein Survivin was shown to contribute to the resistance to EGFR tyrosine kinase inhibitors (TKI) in EGFR mutation-positive NSCLC. However, the unorganized tumor blood vessels impeded drug penetration into tumor tissue. The resulting insufficient intracellular drug/gene delivery in drug-resistant cancer cells remarkably weakened the drug efficacy in NSCLC. In this work, a multi-functional drug delivery system AP/ES was developed by using anti-EGFR aptamer (Apt)-modified polyamidoamine to co-deliver erlotinib and Survivin-shRNA. Chloroquine (CQ) was used in combination with AP/ES to normalize tumor vessels for sufficient drug/gene delivery to overcome drug resistance in NSCLC cells. The obtained AP/ES possessed desired physicochemical properties, good biostability, controlled drug release profiles, and strong selectivity to EGFR-mutated NSCLC mediated by Apt. CQ not only enhanced endosomal escape ability of AP/ES for efficient gene transfection to inhibit Survivin, but also showed strong vessel-normalization ability to improve tumor microcirculation, which further promoted drug delivery and enhanced drug efficacy in erlotinib-resistant NSCLC cells. Our innovative gene/drug co-delivery system in combination with CQ showed a promising outcome in fighting against erlotinib resistance both in vitro and in vivo. This work indicates that normalization of tumor vessels could help intracellular erlotinib/Survivin-shRNA delivery and the down-regulation of Survivin could act synergistically with erlotinib for reversal of erlotinib resistance in EGFR mutation-positive NSCLC.
DOI: 10.1016/j.actbio.2018.06.034
PubMed: 29960010
Links to Exploration step
pubmed:29960010Le document en format XML
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<author><name sortKey="Xu, Liang" sort="Xu, Liang" uniqKey="Xu L" first="Liang" last="Xu">Liang Xu</name>
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<series><title level="j">Acta biomaterialia</title>
<idno type="eISSN">1878-7568</idno>
<imprint><date when="2018" type="published">2018</date>
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<term>Aptamers, Nucleotide (chemistry)</term>
<term>Aptamers, Nucleotide (pharmacokinetics)</term>
<term>Aptamers, Nucleotide (pharmacology)</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>Carcinoma, Non-Small-Cell Lung (pathology)</term>
<term>Cell Line, Tumor</term>
<term>Chloroquine (chemistry)</term>
<term>Chloroquine (pharmacokinetics)</term>
<term>Chloroquine (pharmacology)</term>
<term>Drug Resistance, Neoplasm (drug effects)</term>
<term>Drug Resistance, Neoplasm (genetics)</term>
<term>ErbB Receptors (genetics)</term>
<term>ErbB Receptors (metabolism)</term>
<term>Erlotinib Hydrochloride (chemistry)</term>
<term>Erlotinib Hydrochloride (pharmacokinetics)</term>
<term>Erlotinib Hydrochloride (pharmacology)</term>
<term>Female</term>
<term>Humans</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Lung Neoplasms (genetics)</term>
<term>Lung Neoplasms (metabolism)</term>
<term>Lung Neoplasms (pathology)</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Mice, Nude</term>
<term>Mutation</term>
<term>Nanoparticles (chemistry)</term>
<term>Nanoparticles (therapeutic use)</term>
<term>Neoplasm Proteins (genetics)</term>
<term>Neoplasm Proteins (metabolism)</term>
<term>RNA, Small Interfering (chemistry)</term>
<term>RNA, Small Interfering (pharmacokinetics)</term>
<term>RNA, Small Interfering (pharmacology)</term>
<term>Survivin</term>
<term>Xenograft Model Antitumor Assays</term>
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<term>RNA, Small Interfering</term>
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<term>Neoplasm Proteins</term>
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<term>Chloroquine</term>
<term>Erlotinib Hydrochloride</term>
<term>RNA, Small Interfering</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Aptamers, Nucleotide</term>
<term>Chloroquine</term>
<term>Erlotinib Hydrochloride</term>
<term>RNA, Small Interfering</term>
</keywords>
<keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Nanoparticles</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Drug Resistance, Neoplasm</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>Drug Resistance, Neoplasm</term>
<term>Lung Neoplasms</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung Neoplasms</term>
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<front><div type="abstract" xml:lang="en">Although novel molecular targeted drugs have been recognized as an effective therapy for non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) activating mutations, their efficacy fails to meet the expectation due to the acquired resistance in tumors. Up-regulation of the anti-apoptotic protein Survivin was shown to contribute to the resistance to EGFR tyrosine kinase inhibitors (TKI) in EGFR mutation-positive NSCLC. However, the unorganized tumor blood vessels impeded drug penetration into tumor tissue. The resulting insufficient intracellular drug/gene delivery in drug-resistant cancer cells remarkably weakened the drug efficacy in NSCLC. In this work, a multi-functional drug delivery system AP/ES was developed by using anti-EGFR aptamer (Apt)-modified polyamidoamine to co-deliver erlotinib and Survivin-shRNA. Chloroquine (CQ) was used in combination with AP/ES to normalize tumor vessels for sufficient drug/gene delivery to overcome drug resistance in NSCLC cells. The obtained AP/ES possessed desired physicochemical properties, good biostability, controlled drug release profiles, and strong selectivity to EGFR-mutated NSCLC mediated by Apt. CQ not only enhanced endosomal escape ability of AP/ES for efficient gene transfection to inhibit Survivin, but also showed strong vessel-normalization ability to improve tumor microcirculation, which further promoted drug delivery and enhanced drug efficacy in erlotinib-resistant NSCLC cells. Our innovative gene/drug co-delivery system in combination with CQ showed a promising outcome in fighting against erlotinib resistance both in vitro and in vivo. This work indicates that normalization of tumor vessels could help intracellular erlotinib/Survivin-shRNA delivery and the down-regulation of Survivin could act synergistically with erlotinib for reversal of erlotinib resistance in EGFR mutation-positive NSCLC.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29960010</PMID>
<DateCompleted><Year>2019</Year>
<Month>05</Month>
<Day>22</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>05</Month>
<Day>22</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-7568</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>76</Volume>
<PubDate><Year>2018</Year>
<Month>08</Month>
</PubDate>
</JournalIssue>
<Title>Acta biomaterialia</Title>
<ISOAbbreviation>Acta Biomater</ISOAbbreviation>
</Journal>
<ArticleTitle>Chloroquine in combination with aptamer-modified nanocomplexes for tumor vessel normalization and efficient erlotinib/Survivin shRNA co-delivery to overcome drug resistance in EGFR-mutated non-small cell lung cancer.</ArticleTitle>
<Pagination><MedlinePgn>257-274</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S1742-7061(18)30380-5</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.actbio.2018.06.034</ELocationID>
<Abstract><AbstractText>Although novel molecular targeted drugs have been recognized as an effective therapy for non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) activating mutations, their efficacy fails to meet the expectation due to the acquired resistance in tumors. Up-regulation of the anti-apoptotic protein Survivin was shown to contribute to the resistance to EGFR tyrosine kinase inhibitors (TKI) in EGFR mutation-positive NSCLC. However, the unorganized tumor blood vessels impeded drug penetration into tumor tissue. The resulting insufficient intracellular drug/gene delivery in drug-resistant cancer cells remarkably weakened the drug efficacy in NSCLC. In this work, a multi-functional drug delivery system AP/ES was developed by using anti-EGFR aptamer (Apt)-modified polyamidoamine to co-deliver erlotinib and Survivin-shRNA. Chloroquine (CQ) was used in combination with AP/ES to normalize tumor vessels for sufficient drug/gene delivery to overcome drug resistance in NSCLC cells. The obtained AP/ES possessed desired physicochemical properties, good biostability, controlled drug release profiles, and strong selectivity to EGFR-mutated NSCLC mediated by Apt. CQ not only enhanced endosomal escape ability of AP/ES for efficient gene transfection to inhibit Survivin, but also showed strong vessel-normalization ability to improve tumor microcirculation, which further promoted drug delivery and enhanced drug efficacy in erlotinib-resistant NSCLC cells. Our innovative gene/drug co-delivery system in combination with CQ showed a promising outcome in fighting against erlotinib resistance both in vitro and in vivo. This work indicates that normalization of tumor vessels could help intracellular erlotinib/Survivin-shRNA delivery and the down-regulation of Survivin could act synergistically with erlotinib for reversal of erlotinib resistance in EGFR mutation-positive NSCLC.</AbstractText>
<AbstractText Label="STATEMENT OF SIGNIFICANCE">NSCLC patients who benefited from EGFR-TKIs inevitably developed acquired resistance. Previous research focused on synthesis of new generation of molecular targeted drugs that could irreversibly inhibit EGFR with a particular gene mutation to overcome drug resistance. However, they failed to inhibit EGFR with other gene mutations. Activation of bypass signaling pathway and the changes of tumor microenvironment are identified as two of the mechanisms of acquired resistance to EGFR-TKIs. We therefore constructed multifunctional gene/drug co-delivery nanocomplexes AP/ES co-formulated with chloroquine that could target the both two mechanisms. We found that chloroquine not only enhanced endosomal escape ability of AP/ES for efficient gene transfection to inhibit Survivin, but also showed strong vessel-normalization ability to improve tumor microcirculation, which further promoted drug delivery into tumor tissue and enhanced drug efficacy in erlotinib-resistant NSCLC.</AbstractText>
<CopyrightInformation>Copyright © 2018 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lv</LastName>
<ForeName>Tingting</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Ziying</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Liang</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Yingying</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Haijun</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gao</LastName>
<ForeName>Yu</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China. Electronic address: hellogaoyu@126.com.</Affiliation>
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<Language>eng</Language>
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<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>06</Month>
<Day>28</Day>
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<MedlineTA>Acta Biomater</MedlineTA>
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<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
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<Keyword MajorTopicYN="Y">NSCLC</Keyword>
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<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year>
<Month>02</Month>
<Day>06</Day>
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<PubMedPubDate PubStatus="revised"><Year>2018</Year>
<Month>05</Month>
<Day>23</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2018</Year>
<Month>06</Month>
<Day>26</Day>
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<ArticleIdList><ArticleId IdType="pubmed">29960010</ArticleId>
<ArticleId IdType="pii">S1742-7061(18)30380-5</ArticleId>
<ArticleId IdType="doi">10.1016/j.actbio.2018.06.034</ArticleId>
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