A novel and promising therapeutic approach for NSCLC: recombinant human arginase alone or combined with autophagy inhibitor.
Identifieur interne : 000168 ( PubMed/Corpus ); précédent : 000167; suivant : 000169A novel and promising therapeutic approach for NSCLC: recombinant human arginase alone or combined with autophagy inhibitor.
Auteurs : Weitao Shen ; Xuyao Zhang ; Xiang Fu ; Jiajun Fan ; Jingyun Luan ; Zhonglian Cao ; Ping Yang ; Zhongyuan Xu ; Dianwen JuSource :
- Cell death & disease [ 2041-4889 ] ; 2017.
English descriptors
- KwdEn :
- Apoptosis (drug effects), Arginase (pharmacology), Autophagy (drug effects), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (metabolism), Carcinoma, Non-Small-Cell Lung (pathology), Cell Line, Tumor, Chloroquine (pharmacology), Chromones (pharmacology), Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (metabolism), Lung Neoplasms (pathology), Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (metabolism), Morpholines (pharmacology), Neoplasm Proteins (metabolism), Recombinant Proteins (pharmacology).
- MESH :
- chemical , genetics : Microtubule-Associated Proteins.
- chemical , metabolism : Microtubule-Associated Proteins, Neoplasm Proteins.
- chemical , pharmacology : Arginase, Chloroquine, Chromones, Morpholines, Recombinant Proteins.
- drug effects : Apoptosis, Autophagy.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- metabolism : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- Cell Line, Tumor, Humans.
Abstract
Recombinant human arginase (rhArg), an enzyme capable of depleting arginine, has been shown to be an effective therapeutic approach for various cancers. Non-small-cell lung cancer (NSCLC), a histological subtype of pulmonary carcinoma, has a high rate of morbidity and mortality in the world. Thus, the need for novel and more effective treatment is urgent. In this study, it is the first time to report that rhArg could induce significant cytotoxicity and caspase-dependent apoptosis in NSCLC cells. Subsequently, our research revealed that rhArg dramatically stimulated autophagic response in NSCLC cells, which was proved by the formation and accumulation of autophagosomes and the conversion of microtubule-associated protein light chain 3 (LC3) from LC3-I to LC3-II. Furthermore, blocking autophagy by chloroquine or LY294002 remarkably enhanced rhArg-induced cytotoxicity and caspase-dependent apoptosis, suggesting that autophagy acted a cytoprotective role in rhArg-treated NSCLC cells. Further experiments showed that two signaling pathways including the Akt/mTOR and extracellular signal-regulated kinase pathway, and mitochondrial-derived reactive oxygen species (ROS) production were involved in rhArg-induced autophagy and apoptosis. Meanwhile, N-acetyl-L-cysteine, a common antioxidant, was employed to scavenge ROS, and we detected that it could significantly block rhArg-induced autophagy and cytotoxicity, indicating that ROS played a vital role in arginine degradation therapy. Besides, xenograft experiment showed that combination with autophagy inhibitor potentiated the anti-tumor efficacy of rhArg in vivo. Therefore, these results provided a novel prospect and viewpoint that autophagy acted a cytoprotective role in rhArg-treated NSCLC cells, and treatment with rhArg alone or combined with autophagy inhibitor could be a novel and promising therapeutic approach for NSCLC in vivo and in vitro.
DOI: 10.1038/cddis.2017.137
PubMed: 28358368
Links to Exploration step
pubmed:28358368Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">A novel and promising therapeutic approach for NSCLC: recombinant human arginase alone or combined with autophagy inhibitor.</title><author><name sortKey="Shen, Weitao" sort="Shen, Weitao" uniqKey="Shen W" first="Weitao" last="Shen">Weitao Shen</name><affiliation><nlm:affiliation>Department of Research Center for Clinical Pharmacology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Xuyao" sort="Zhang, Xuyao" uniqKey="Zhang X" first="Xuyao" last="Zhang">Xuyao Zhang</name><affiliation><nlm:affiliation>Department of Microbiological and Biochemical Pharmacy & The Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, Shanghai 201203, China.</nlm:affiliation></affiliation></author><author><name sortKey="Fu, Xiang" sort="Fu, Xiang" uniqKey="Fu X" first="Xiang" last="Fu">Xiang Fu</name><affiliation><nlm:affiliation>Department of Research Center for Clinical Pharmacology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.</nlm:affiliation></affiliation></author><author><name sortKey="Fan, Jiajun" sort="Fan, Jiajun" uniqKey="Fan J" first="Jiajun" last="Fan">Jiajun Fan</name><affiliation><nlm:affiliation>Department of Microbiological and Biochemical Pharmacy & The Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, Shanghai 201203, China.</nlm:affiliation></affiliation></author><author><name sortKey="Luan, Jingyun" sort="Luan, Jingyun" uniqKey="Luan J" first="Jingyun" last="Luan">Jingyun Luan</name><affiliation><nlm:affiliation>Department of Microbiological and Biochemical Pharmacy & The Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, Shanghai 201203, China.</nlm:affiliation></affiliation></author><author><name sortKey="Cao, Zhonglian" 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Shen</name><affiliation><nlm:affiliation>Department of Research Center for Clinical Pharmacology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Xuyao" sort="Zhang, Xuyao" uniqKey="Zhang X" first="Xuyao" last="Zhang">Xuyao Zhang</name><affiliation><nlm:affiliation>Department of Microbiological and Biochemical Pharmacy & The Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, Shanghai 201203, China.</nlm:affiliation></affiliation></author><author><name sortKey="Fu, Xiang" sort="Fu, Xiang" uniqKey="Fu X" first="Xiang" last="Fu">Xiang Fu</name><affiliation><nlm:affiliation>Department of Research Center for Clinical Pharmacology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.</nlm:affiliation></affiliation></author><author><name sortKey="Fan, Jiajun" sort="Fan, Jiajun" uniqKey="Fan J" first="Jiajun" last="Fan">Jiajun Fan</name><affiliation><nlm:affiliation>Department of Microbiological and Biochemical Pharmacy & The Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, Shanghai 201203, China.</nlm:affiliation></affiliation></author><author><name sortKey="Luan, Jingyun" sort="Luan, Jingyun" uniqKey="Luan J" first="Jingyun" last="Luan">Jingyun Luan</name><affiliation><nlm:affiliation>Department of Microbiological and Biochemical Pharmacy & The Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, Shanghai 201203, China.</nlm:affiliation></affiliation></author><author><name sortKey="Cao, Zhonglian" sort="Cao, Zhonglian" uniqKey="Cao Z" first="Zhonglian" last="Cao">Zhonglian Cao</name><affiliation><nlm:affiliation>Department of Instrumental Analysis Center, School of Pharmacy, Fudan University, Shanghai 201203, China.</nlm:affiliation></affiliation></author><author><name sortKey="Yang, Ping" sort="Yang, Ping" uniqKey="Yang P" first="Ping" last="Yang">Ping Yang</name><affiliation><nlm:affiliation>Department of Instrumental Analysis Center, School of Pharmacy, Fudan University, Shanghai 201203, China.</nlm:affiliation></affiliation></author><author><name sortKey="Xu, Zhongyuan" sort="Xu, Zhongyuan" uniqKey="Xu Z" first="Zhongyuan" last="Xu">Zhongyuan Xu</name><affiliation><nlm:affiliation>Department of Research Center for Clinical Pharmacology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.</nlm:affiliation></affiliation></author><author><name sortKey="Ju, Dianwen" sort="Ju, Dianwen" uniqKey="Ju D" first="Dianwen" last="Ju">Dianwen Ju</name><affiliation><nlm:affiliation>Department of Microbiological and Biochemical Pharmacy & The Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, Shanghai 201203, China.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Cell death & disease</title><idno type="eISSN">2041-4889</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis (drug effects)</term><term>Arginase (pharmacology)</term><term>Autophagy (drug effects)</term><term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term><term>Carcinoma, Non-Small-Cell Lung (metabolism)</term><term>Carcinoma, Non-Small-Cell Lung (pathology)</term><term>Cell Line, Tumor</term><term>Chloroquine (pharmacology)</term><term>Chromones (pharmacology)</term><term>Humans</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (metabolism)</term><term>Lung Neoplasms (pathology)</term><term>Microtubule-Associated Proteins (genetics)</term><term>Microtubule-Associated Proteins (metabolism)</term><term>Morpholines (pharmacology)</term><term>Neoplasm Proteins (metabolism)</term><term>Recombinant Proteins (pharmacology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Microtubule-Associated Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Microtubule-Associated Proteins</term><term>Neoplasm Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Arginase</term><term>Chloroquine</term><term>Chromones</term><term>Morpholines</term><term>Recombinant Proteins</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</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="metabolism" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Recombinant human arginase (rhArg), an enzyme capable of depleting arginine, has been shown to be an effective therapeutic approach for various cancers. Non-small-cell lung cancer (NSCLC), a histological subtype of pulmonary carcinoma, has a high rate of morbidity and mortality in the world. Thus, the need for novel and more effective treatment is urgent. In this study, it is the first time to report that rhArg could induce significant cytotoxicity and caspase-dependent apoptosis in NSCLC cells. Subsequently, our research revealed that rhArg dramatically stimulated autophagic response in NSCLC cells, which was proved by the formation and accumulation of autophagosomes and the conversion of microtubule-associated protein light chain 3 (LC3) from LC3-I to LC3-II. Furthermore, blocking autophagy by chloroquine or LY294002 remarkably enhanced rhArg-induced cytotoxicity and caspase-dependent apoptosis, suggesting that autophagy acted a cytoprotective role in rhArg-treated NSCLC cells. Further experiments showed that two signaling pathways including the Akt/mTOR and extracellular signal-regulated kinase pathway, and mitochondrial-derived reactive oxygen species (ROS) production were involved in rhArg-induced autophagy and apoptosis. Meanwhile, N-acetyl-L-cysteine, a common antioxidant, was employed to scavenge ROS, and we detected that it could significantly block rhArg-induced autophagy and cytotoxicity, indicating that ROS played a vital role in arginine degradation therapy. Besides, xenograft experiment showed that combination with autophagy inhibitor potentiated the anti-tumor efficacy of rhArg in vivo. Therefore, these results provided a novel prospect and viewpoint that autophagy acted a cytoprotective role in rhArg-treated NSCLC cells, and treatment with rhArg alone or combined with autophagy inhibitor could be a novel and promising therapeutic approach for NSCLC in vivo and in vitro.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28358368</PMID><DateCompleted><Year>2017</Year><Month>11</Month><Day>20</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2041-4889</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><Issue>3</Issue><PubDate><Year>2017</Year><Month>03</Month><Day>30</Day></PubDate></JournalIssue><Title>Cell death & disease</Title><ISOAbbreviation>Cell Death Dis</ISOAbbreviation></Journal><ArticleTitle>A novel and promising therapeutic approach for NSCLC: recombinant human arginase alone or combined with autophagy inhibitor.</ArticleTitle><Pagination><MedlinePgn>e2720</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/cddis.2017.137</ELocationID><Abstract><AbstractText>Recombinant human arginase (rhArg), an enzyme capable of depleting arginine, has been shown to be an effective therapeutic approach for various cancers. Non-small-cell lung cancer (NSCLC), a histological subtype of pulmonary carcinoma, has a high rate of morbidity and mortality in the world. Thus, the need for novel and more effective treatment is urgent. In this study, it is the first time to report that rhArg could induce significant cytotoxicity and caspase-dependent apoptosis in NSCLC cells. Subsequently, our research revealed that rhArg dramatically stimulated autophagic response in NSCLC cells, which was proved by the formation and accumulation of autophagosomes and the conversion of microtubule-associated protein light chain 3 (LC3) from LC3-I to LC3-II. Furthermore, blocking autophagy by chloroquine or LY294002 remarkably enhanced rhArg-induced cytotoxicity and caspase-dependent apoptosis, suggesting that autophagy acted a cytoprotective role in rhArg-treated NSCLC cells. Further experiments showed that two signaling pathways including the Akt/mTOR and extracellular signal-regulated kinase pathway, and mitochondrial-derived reactive oxygen species (ROS) production were involved in rhArg-induced autophagy and apoptosis. Meanwhile, N-acetyl-L-cysteine, a common antioxidant, was employed to scavenge ROS, and we detected that it could significantly block rhArg-induced autophagy and cytotoxicity, indicating that ROS played a vital role in arginine degradation therapy. Besides, xenograft experiment showed that combination with autophagy inhibitor potentiated the anti-tumor efficacy of rhArg in vivo. Therefore, these results provided a novel prospect and viewpoint that autophagy acted a cytoprotective role in rhArg-treated NSCLC cells, and treatment with rhArg alone or combined with autophagy inhibitor could be a novel and promising therapeutic approach for NSCLC in vivo and in vitro.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shen</LastName><ForeName>Weitao</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Research Center for Clinical Pharmacology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Xuyao</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Microbiological and Biochemical Pharmacy & The Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, Shanghai 201203, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fu</LastName><ForeName>Xiang</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Research Center for Clinical Pharmacology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fan</LastName><ForeName>Jiajun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Microbiological and Biochemical Pharmacy & The Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, Shanghai 201203, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Luan</LastName><ForeName>Jingyun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Microbiological and Biochemical Pharmacy & The Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, Shanghai 201203, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cao</LastName><ForeName>Zhonglian</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Instrumental Analysis Center, School of Pharmacy, Fudan University, Shanghai 201203, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Ping</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Instrumental Analysis Center, School of Pharmacy, Fudan University, Shanghai 201203, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Zhongyuan</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Research Center for Clinical Pharmacology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ju</LastName><ForeName>Dianwen</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Microbiological and Biochemical Pharmacy & The Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, Shanghai 201203, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>03</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cell Death Dis</MedlineTA><NlmUniqueID>101524092</NlmUniqueID></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002867">Chromones</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C477012">MAP1LC3A protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008869">Microtubule-Associated Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009025">Morpholines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009363">Neoplasm Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011994">Recombinant Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>31M2U1DVID</RegistryNumber><NameOfSubstance UI="C085911">2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.5.3.1</RegistryNumber><NameOfSubstance UI="D001119">Arginase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001119" MajorTopicYN="N">Arginase</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002289" MajorTopicYN="N">Carcinoma, Non-Small-Cell Lung</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002867" MajorTopicYN="N">Chromones</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</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="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008869" MajorTopicYN="N">Microtubule-Associated Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009025" MajorTopicYN="N">Morpholines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009363" MajorTopicYN="N">Neoplasm Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011994" MajorTopicYN="N">Recombinant Proteins</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>11</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>02</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>02</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>3</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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