Novel dihydroartemisinin derivative DHA-37 induces autophagic cell death through upregulation of HMGB1 in A549 cells.
Identifieur interne : 000080 ( PubMed/Curation ); précédent : 000079; suivant : 000081Novel dihydroartemisinin derivative DHA-37 induces autophagic cell death through upregulation of HMGB1 in A549 cells.
Auteurs : Xiufeng Liu [République populaire de Chine] ; Juanjuan Wu [République populaire de Chine] ; Menglin Fan [République populaire de Chine] ; Chen Shen [République populaire de Chine] ; Wenling Dai [République populaire de Chine] ; Yini Bao [République populaire de Chine] ; Ji-Hua Liu [République populaire de Chine] ; Bo-Yang Yu [République populaire de Chine]Source :
- Cell death & disease [ 2041-4889 ] ; 2018.
Descripteurs français
- KwdFr :
- Adénocarcinome bronchioloalvéolaire (anatomopathologie), Adénocarcinome bronchioloalvéolaire (génétique), Adénocarcinome bronchioloalvéolaire (métabolisme), Adénocarcinome bronchioloalvéolaire (traitement médicamenteux), Animaux, Antinéoplasiques d'origine végétale (pharmacologie), Antinéoplasiques d'origine végétale (synthèse chimique), Artémisinines (pharmacologie), Artémisinines (synthèse chimique), Autophagie (), Autophagie (génétique), Cellules A549, Charge tumorale (), Cycle cellulaire (), Cycle cellulaire (génétique), Humains, Mitogen-Activated Protein Kinase 1 (génétique), Mitogen-Activated Protein Kinase 1 (métabolisme), Mitogen-Activated Protein Kinase 3 (génétique), Mitogen-Activated Protein Kinase 3 (métabolisme), Mitogen-Activated Protein Kinase 8 (génétique), Mitogen-Activated Protein Kinase 8 (métabolisme), Mâle, Petit ARN interférent (génétique), Petit ARN interférent (métabolisme), Protéine HMGB1 (antagonistes et inhibiteurs), Protéine HMGB1 (génétique), Protéine HMGB1 (métabolisme), Protéines associées aux microtubules (génétique), Protéines associées aux microtubules (métabolisme), Régulation de l'expression des gènes tumoraux, Souris, Souris nude, Tests d'activité antitumorale sur modèle de xénogreffe, Transduction du signal, Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (génétique), Tumeurs du poumon (métabolisme), Tumeurs du poumon (traitement médicamenteux), Vacuoles (), Vacuoles (métabolisme), Vacuoles (ultrastructure).
- MESH :
- anatomopathologie : Adénocarcinome bronchioloalvéolaire, Tumeurs du poumon.
- antagonistes et inhibiteurs : Protéine HMGB1.
- génétique : Adénocarcinome bronchioloalvéolaire, Autophagie, Cycle cellulaire, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Mitogen-Activated Protein Kinase 8, Petit ARN interférent, Protéine HMGB1, Protéines associées aux microtubules, Tumeurs du poumon.
- métabolisme : Adénocarcinome bronchioloalvéolaire, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Mitogen-Activated Protein Kinase 8, Petit ARN interférent, Protéine HMGB1, Protéines associées aux microtubules, Tumeurs du poumon, Vacuoles.
- pharmacologie : Antinéoplasiques d'origine végétale, Artémisinines.
- synthèse chimique : Antinéoplasiques d'origine végétale, Artémisinines.
- traitement médicamenteux : Adénocarcinome bronchioloalvéolaire, Tumeurs du poumon.
- Animaux, Autophagie, Cellules A549, Charge tumorale, Cycle cellulaire, Humains, Mâle, Régulation de l'expression des gènes tumoraux, Souris, Souris nude, Tests d'activité antitumorale sur modèle de xénogreffe, Transduction du signal, Vacuoles.
English descriptors
- KwdEn :
- A549 Cells, Adenocarcinoma, Bronchiolo-Alveolar (drug therapy), Adenocarcinoma, Bronchiolo-Alveolar (genetics), Adenocarcinoma, Bronchiolo-Alveolar (metabolism), Adenocarcinoma, Bronchiolo-Alveolar (pathology), Animals, Antineoplastic Agents, Phytogenic (chemical synthesis), Antineoplastic Agents, Phytogenic (pharmacology), Artemisinins (chemical synthesis), Artemisinins (pharmacology), Autophagy (drug effects), Autophagy (genetics), Cell Cycle (drug effects), Cell Cycle (genetics), Gene Expression Regulation, Neoplastic, HMGB1 Protein (antagonists & inhibitors), HMGB1 Protein (genetics), HMGB1 Protein (metabolism), Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (metabolism), Lung Neoplasms (pathology), Male, Mice, Mice, Nude, Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (metabolism), Mitogen-Activated Protein Kinase 1 (genetics), Mitogen-Activated Protein Kinase 1 (metabolism), Mitogen-Activated Protein Kinase 3 (genetics), Mitogen-Activated Protein Kinase 3 (metabolism), Mitogen-Activated Protein Kinase 8 (genetics), Mitogen-Activated Protein Kinase 8 (metabolism), RNA, Small Interfering (genetics), RNA, Small Interfering (metabolism), Signal Transduction, Tumor Burden (drug effects), Vacuoles (drug effects), Vacuoles (metabolism), Vacuoles (ultrastructure), Xenograft Model Antitumor Assays.
- MESH :
- chemical , antagonists & inhibitors : HMGB1 Protein.
- chemical , chemical synthesis : Antineoplastic Agents, Phytogenic, Artemisinins.
- drug effects : Autophagy, Cell Cycle, Tumor Burden, Vacuoles.
- drug therapy : Adenocarcinoma, Bronchiolo-Alveolar, Lung Neoplasms.
- genetics : Adenocarcinoma, Bronchiolo-Alveolar, Autophagy, Cell Cycle, HMGB1 Protein, Lung Neoplasms, Microtubule-Associated Proteins, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Mitogen-Activated Protein Kinase 8, RNA, Small Interfering.
- metabolism : Adenocarcinoma, Bronchiolo-Alveolar, HMGB1 Protein, Lung Neoplasms, Microtubule-Associated Proteins, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Mitogen-Activated Protein Kinase 8, RNA, Small Interfering, Vacuoles.
- pathology : Adenocarcinoma, Bronchiolo-Alveolar, Lung Neoplasms.
- chemical , pharmacology : Antineoplastic Agents, Phytogenic, Artemisinins.
- ultrastructure : Vacuoles.
- A549 Cells, Animals, Gene Expression Regulation, Neoplastic, Humans, Male, Mice, Mice, Nude, Signal Transduction, Xenograft Model Antitumor Assays.
Abstract
Dihydroartemisinin (DHA) and its analogs are reported to possess selective anticancer activity. Here, we reported a novel DHA derivative DHA-37 that exhibited more potent anticancer activity on the cells tested. Distinct from DHA-induced apoptosis, DHA-37 triggered excessive autophagic cell death, and became the main contributor to DHA-37-induced A549 cell death. Incubation of the cells with DHA-37 but not DHA produced increased dots distribution of GFP-LC3 and expression ratio of LC3-II/LC3-I, and enhanced the formation of autophagic vacuoles as revealed by TEM. Treatment with the autophagy inhibitor 3-MA, LY294002, or chloroquine could reverse DHA-37-induced cell death. In addition, DHA-37-induced cell death was associated significantly with the increased expression of HMGB1, and knockdown of HMGB1 could reverse DHA-37-induced cell death. More importantly, the elevated HMGB1 expression induced autophagy through the activation of the MAPK signal but not PI3K-AKT-mTOR pathway. In addition, DHA-37 also showed a wonderful performance in A549 xenograft mice model. These findings suggest that HMGB1 as a target candidate for apoptosis-resistant cancer treatment and artemisinin-based drugs could be used in inducing autophagic cell death.
DOI: 10.1038/s41419-018-1006-y
PubMed: 30323180
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A549 Cells</term>
<term>Adenocarcinoma, Bronchiolo-Alveolar (drug therapy)</term>
<term>Adenocarcinoma, Bronchiolo-Alveolar (genetics)</term>
<term>Adenocarcinoma, Bronchiolo-Alveolar (metabolism)</term>
<term>Adenocarcinoma, Bronchiolo-Alveolar (pathology)</term>
<term>Animals</term>
<term>Antineoplastic Agents, Phytogenic (chemical synthesis)</term>
<term>Antineoplastic Agents, Phytogenic (pharmacology)</term>
<term>Artemisinins (chemical synthesis)</term>
<term>Artemisinins (pharmacology)</term>
<term>Autophagy (drug effects)</term>
<term>Autophagy (genetics)</term>
<term>Cell Cycle (drug effects)</term>
<term>Cell Cycle (genetics)</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>HMGB1 Protein (antagonists & inhibitors)</term>
<term>HMGB1 Protein (genetics)</term>
<term>HMGB1 Protein (metabolism)</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>Male</term>
<term>Mice</term>
<term>Mice, Nude</term>
<term>Microtubule-Associated Proteins (genetics)</term>
<term>Microtubule-Associated Proteins (metabolism)</term>
<term>Mitogen-Activated Protein Kinase 1 (genetics)</term>
<term>Mitogen-Activated Protein Kinase 1 (metabolism)</term>
<term>Mitogen-Activated Protein Kinase 3 (genetics)</term>
<term>Mitogen-Activated Protein Kinase 3 (metabolism)</term>
<term>Mitogen-Activated Protein Kinase 8 (genetics)</term>
<term>Mitogen-Activated Protein Kinase 8 (metabolism)</term>
<term>RNA, Small Interfering (genetics)</term>
<term>RNA, Small Interfering (metabolism)</term>
<term>Signal Transduction</term>
<term>Tumor Burden (drug effects)</term>
<term>Vacuoles (drug effects)</term>
<term>Vacuoles (metabolism)</term>
<term>Vacuoles (ultrastructure)</term>
<term>Xenograft Model Antitumor Assays</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Adénocarcinome bronchioloalvéolaire (anatomopathologie)</term>
<term>Adénocarcinome bronchioloalvéolaire (génétique)</term>
<term>Adénocarcinome bronchioloalvéolaire (métabolisme)</term>
<term>Adénocarcinome bronchioloalvéolaire (traitement médicamenteux)</term>
<term>Animaux</term>
<term>Antinéoplasiques d'origine végétale (pharmacologie)</term>
<term>Antinéoplasiques d'origine végétale (synthèse chimique)</term>
<term>Artémisinines (pharmacologie)</term>
<term>Artémisinines (synthèse chimique)</term>
<term>Autophagie ()</term>
<term>Autophagie (génétique)</term>
<term>Cellules A549</term>
<term>Charge tumorale ()</term>
<term>Cycle cellulaire ()</term>
<term>Cycle cellulaire (génétique)</term>
<term>Humains</term>
<term>Mitogen-Activated Protein Kinase 1 (génétique)</term>
<term>Mitogen-Activated Protein Kinase 1 (métabolisme)</term>
<term>Mitogen-Activated Protein Kinase 3 (génétique)</term>
<term>Mitogen-Activated Protein Kinase 3 (métabolisme)</term>
<term>Mitogen-Activated Protein Kinase 8 (génétique)</term>
<term>Mitogen-Activated Protein Kinase 8 (métabolisme)</term>
<term>Mâle</term>
<term>Petit ARN interférent (génétique)</term>
<term>Petit ARN interférent (métabolisme)</term>
<term>Protéine HMGB1 (antagonistes et inhibiteurs)</term>
<term>Protéine HMGB1 (génétique)</term>
<term>Protéine HMGB1 (métabolisme)</term>
<term>Protéines associées aux microtubules (génétique)</term>
<term>Protéines associées aux microtubules (métabolisme)</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Souris</term>
<term>Souris nude</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe</term>
<term>Transduction du signal</term>
<term>Tumeurs du poumon (anatomopathologie)</term>
<term>Tumeurs du poumon (génétique)</term>
<term>Tumeurs du poumon (métabolisme)</term>
<term>Tumeurs du poumon (traitement médicamenteux)</term>
<term>Vacuoles ()</term>
<term>Vacuoles (métabolisme)</term>
<term>Vacuoles (ultrastructure)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>HMGB1 Protein</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="chemical synthesis" xml:lang="en"><term>Antineoplastic Agents, Phytogenic</term>
<term>Artemisinins</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Adénocarcinome bronchioloalvéolaire</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Protéine HMGB1</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term>
<term>Cell Cycle</term>
<term>Tumor Burden</term>
<term>Vacuoles</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Adenocarcinoma, Bronchiolo-Alveolar</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adenocarcinoma, Bronchiolo-Alveolar</term>
<term>Autophagy</term>
<term>Cell Cycle</term>
<term>HMGB1 Protein</term>
<term>Lung Neoplasms</term>
<term>Microtubule-Associated Proteins</term>
<term>Mitogen-Activated Protein Kinase 1</term>
<term>Mitogen-Activated Protein Kinase 3</term>
<term>Mitogen-Activated Protein Kinase 8</term>
<term>RNA, Small Interfering</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Adénocarcinome bronchioloalvéolaire</term>
<term>Autophagie</term>
<term>Cycle cellulaire</term>
<term>Mitogen-Activated Protein Kinase 1</term>
<term>Mitogen-Activated Protein Kinase 3</term>
<term>Mitogen-Activated Protein Kinase 8</term>
<term>Petit ARN interférent</term>
<term>Protéine HMGB1</term>
<term>Protéines associées aux microtubules</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Adenocarcinoma, Bronchiolo-Alveolar</term>
<term>HMGB1 Protein</term>
<term>Lung Neoplasms</term>
<term>Microtubule-Associated Proteins</term>
<term>Mitogen-Activated Protein Kinase 1</term>
<term>Mitogen-Activated Protein Kinase 3</term>
<term>Mitogen-Activated Protein Kinase 8</term>
<term>RNA, Small Interfering</term>
<term>Vacuoles</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Adénocarcinome bronchioloalvéolaire</term>
<term>Mitogen-Activated Protein Kinase 1</term>
<term>Mitogen-Activated Protein Kinase 3</term>
<term>Mitogen-Activated Protein Kinase 8</term>
<term>Petit ARN interférent</term>
<term>Protéine HMGB1</term>
<term>Protéines associées aux microtubules</term>
<term>Tumeurs du poumon</term>
<term>Vacuoles</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Adenocarcinoma, Bronchiolo-Alveolar</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques d'origine végétale</term>
<term>Artémisinines</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents, Phytogenic</term>
<term>Artemisinins</term>
</keywords>
<keywords scheme="MESH" qualifier="synthèse chimique" xml:lang="fr"><term>Antinéoplasiques d'origine végétale</term>
<term>Artémisinines</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Adénocarcinome bronchioloalvéolaire</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Vacuoles</term>
</keywords>
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<term>Animals</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>Humans</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Nude</term>
<term>Signal Transduction</term>
<term>Xenograft Model Antitumor Assays</term>
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<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Autophagie</term>
<term>Cellules A549</term>
<term>Charge tumorale</term>
<term>Cycle cellulaire</term>
<term>Humains</term>
<term>Mâle</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Souris</term>
<term>Souris nude</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe</term>
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<front><div type="abstract" xml:lang="en">Dihydroartemisinin (DHA) and its analogs are reported to possess selective anticancer activity. Here, we reported a novel DHA derivative DHA-37 that exhibited more potent anticancer activity on the cells tested. Distinct from DHA-induced apoptosis, DHA-37 triggered excessive autophagic cell death, and became the main contributor to DHA-37-induced A549 cell death. Incubation of the cells with DHA-37 but not DHA produced increased dots distribution of GFP-LC3 and expression ratio of LC3-II/LC3-I, and enhanced the formation of autophagic vacuoles as revealed by TEM. Treatment with the autophagy inhibitor 3-MA, LY294002, or chloroquine could reverse DHA-37-induced cell death. In addition, DHA-37-induced cell death was associated significantly with the increased expression of HMGB1, and knockdown of HMGB1 could reverse DHA-37-induced cell death. More importantly, the elevated HMGB1 expression induced autophagy through the activation of the MAPK signal but not PI3K-AKT-mTOR pathway. In addition, DHA-37 also showed a wonderful performance in A549 xenograft mice model. These findings suggest that HMGB1 as a target candidate for apoptosis-resistant cancer treatment and artemisinin-based drugs could be used in inducing autophagic cell death.</div>
</front>
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<DateCompleted><Year>2019</Year>
<Month>12</Month>
<Day>10</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>12</Month>
<Day>17</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2041-4889</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>9</Volume>
<Issue>11</Issue>
<PubDate><Year>2018</Year>
<Month>10</Month>
<Day>15</Day>
</PubDate>
</JournalIssue>
<Title>Cell death & disease</Title>
<ISOAbbreviation>Cell Death Dis</ISOAbbreviation>
</Journal>
<ArticleTitle>Novel dihydroartemisinin derivative DHA-37 induces autophagic cell death through upregulation of HMGB1 in A549 cells.</ArticleTitle>
<Pagination><MedlinePgn>1048</MedlinePgn>
</Pagination>
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<Abstract><AbstractText>Dihydroartemisinin (DHA) and its analogs are reported to possess selective anticancer activity. Here, we reported a novel DHA derivative DHA-37 that exhibited more potent anticancer activity on the cells tested. Distinct from DHA-induced apoptosis, DHA-37 triggered excessive autophagic cell death, and became the main contributor to DHA-37-induced A549 cell death. Incubation of the cells with DHA-37 but not DHA produced increased dots distribution of GFP-LC3 and expression ratio of LC3-II/LC3-I, and enhanced the formation of autophagic vacuoles as revealed by TEM. Treatment with the autophagy inhibitor 3-MA, LY294002, or chloroquine could reverse DHA-37-induced cell death. In addition, DHA-37-induced cell death was associated significantly with the increased expression of HMGB1, and knockdown of HMGB1 could reverse DHA-37-induced cell death. More importantly, the elevated HMGB1 expression induced autophagy through the activation of the MAPK signal but not PI3K-AKT-mTOR pathway. In addition, DHA-37 also showed a wonderful performance in A549 xenograft mice model. These findings suggest that HMGB1 as a target candidate for apoptosis-resistant cancer treatment and artemisinin-based drugs could be used in inducing autophagic cell death.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Xiufeng</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Natural Medicines, School of Traditional Chinese Pharmacy, China Pharmaceutical University, 210009, Nanjing, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, 210009, Nanjing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Juanjuan</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Natural Medicines, School of Traditional Chinese Pharmacy, China Pharmaceutical University, 210009, Nanjing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fan</LastName>
<ForeName>Menglin</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Natural Medicines, School of Traditional Chinese Pharmacy, China Pharmaceutical University, 210009, Nanjing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shen</LastName>
<ForeName>Chen</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Natural Medicines, School of Traditional Chinese Pharmacy, China Pharmaceutical University, 210009, Nanjing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dai</LastName>
<ForeName>Wenling</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Natural Medicines, School of Traditional Chinese Pharmacy, China Pharmaceutical University, 210009, Nanjing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bao</LastName>
<ForeName>Yini</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Natural Medicines, School of Traditional Chinese Pharmacy, China Pharmaceutical University, 210009, Nanjing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Ji-Hua</ForeName>
<Initials>JH</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Natural Medicines, School of Traditional Chinese Pharmacy, China Pharmaceutical University, 210009, Nanjing, China. liujihua@cpu.edu.cn.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, 210009, Nanjing, China. liujihua@cpu.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yu</LastName>
<ForeName>Bo-Yang</ForeName>
<Initials>BY</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Natural Medicines, School of Traditional Chinese Pharmacy, China Pharmaceutical University, 210009, Nanjing, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, 210009, Nanjing, 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>2018</Year>
<Month>10</Month>
<Day>15</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Cell Death Dis</MedlineTA>
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<Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber>
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<Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D002282" MajorTopicYN="N">Adenocarcinoma, Bronchiolo-Alveolar</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
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<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002453" MajorTopicYN="N">Cell Cycle</DescriptorName>
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<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015972" MajorTopicYN="Y">Gene Expression Regulation, Neoplastic</DescriptorName>
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<MeshHeading><DescriptorName UI="D024243" MajorTopicYN="N">HMGB1 Protein</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</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>
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<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
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<MeshHeading><DescriptorName UI="D047368" MajorTopicYN="N">Tumor Burden</DescriptorName>
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