Gambogic acid improves non-small cell lung cancer progression by inhibition of mTOR signaling pathway.
Identifieur interne : 000143 ( PubMed/Curation ); précédent : 000142; suivant : 000144Gambogic acid improves non-small cell lung cancer progression by inhibition of mTOR signaling pathway.
Auteurs : Teng Zhao [République populaire de Chine] ; Hong-Jian Wang [République populaire de Chine] ; Wen-Wen Zhao [République populaire de Chine] ; Yi-Ling Sun [République populaire de Chine] ; Li-Kuan Hu [République populaire de Chine]Source :
- The Kaohsiung journal of medical sciences [ 2410-8650 ] ; 2017.
Descripteurs français
- KwdFr :
- Adénine (analogues et dérivés), Adénine (pharmacologie), Antinéoplasiques d'origine végétale (isolement et purification), Antinéoplasiques d'origine végétale (pharmacologie), Association médicamenteuse, Autophagie (), Autophagie (génétique), Cellules A549, Chloroquine (pharmacologie), Cisplatine (pharmacologie), Extraits de plantes (), Garcinia (), Humains, Lignée cellulaire tumorale, Prolifération cellulaire (), Protéine ribosomique S6 (antagonistes et inhibiteurs), Protéine ribosomique S6 (génétique), Protéine ribosomique S6 (métabolisme), Protéines associées aux microtubules (génétique), Protéines associées aux microtubules (métabolisme), Protéines proto-oncogènes c-akt (antagonistes et inhibiteurs), Protéines proto-oncogènes c-akt (génétique), Protéines proto-oncogènes c-akt (métabolisme), Régulation de l'expression des gènes tumoraux, Sirolimus (pharmacologie), Synergie des médicaments, Sérine-thréonine kinases TOR (antagonistes et inhibiteurs), Sérine-thréonine kinases TOR (génétique), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal, Xanthones (isolement et purification), Xanthones (pharmacologie).
- MESH :
- analogues et dérivés : Adénine.
- antagonistes et inhibiteurs : Protéine ribosomique S6, Protéines proto-oncogènes c-akt, Sérine-thréonine kinases TOR.
- génétique : Autophagie, Protéine ribosomique S6, Protéines associées aux microtubules, Protéines proto-oncogènes c-akt, Sérine-thréonine kinases TOR.
- isolement et purification : Antinéoplasiques d'origine végétale, Xanthones.
- métabolisme : Protéine ribosomique S6, Protéines associées aux microtubules, Protéines proto-oncogènes c-akt, Sérine-thréonine kinases TOR.
- pharmacologie : Adénine, Antinéoplasiques d'origine végétale, Chloroquine, Cisplatine, Sirolimus, Xanthones.
- Association médicamenteuse, Autophagie, Cellules A549, Extraits de plantes, Garcinia, Humains, Lignée cellulaire tumorale, Prolifération cellulaire, Régulation de l'expression des gènes tumoraux, Synergie des médicaments, Transduction du signal.
English descriptors
- KwdEn :
- A549 Cells, Adenine (analogs & derivatives), Adenine (pharmacology), Antineoplastic Agents, Phytogenic (isolation & purification), Antineoplastic Agents, Phytogenic (pharmacology), Autophagy (drug effects), Autophagy (genetics), Cell Line, Tumor, Cell Proliferation (drug effects), Chloroquine (pharmacology), Cisplatin (pharmacology), Drug Combinations, Drug Synergism, Garcinia (chemistry), Gene Expression Regulation, Neoplastic, Humans, Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (metabolism), Plant Extracts (chemistry), Proto-Oncogene Proteins c-akt (antagonists & inhibitors), Proto-Oncogene Proteins c-akt (genetics), Proto-Oncogene Proteins c-akt (metabolism), Ribosomal Protein S6 (antagonists & inhibitors), Ribosomal Protein S6 (genetics), Ribosomal Protein S6 (metabolism), Signal Transduction, Sirolimus (pharmacology), TOR Serine-Threonine Kinases (antagonists & inhibitors), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (metabolism), Xanthones (isolation & purification), Xanthones (pharmacology).
- MESH :
- chemical , analogs & derivatives : Adenine.
- chemical , antagonists & inhibitors : Proto-Oncogene Proteins c-akt, Ribosomal Protein S6, TOR Serine-Threonine Kinases.
- chemical , chemistry : Plant Extracts.
- chemical , genetics : Microtubule-Associated Proteins, Proto-Oncogene Proteins c-akt, Ribosomal Protein S6, TOR Serine-Threonine Kinases.
- chemical , isolation & purification : Antineoplastic Agents, Phytogenic, Xanthones.
- chemical , metabolism : Microtubule-Associated Proteins, Proto-Oncogene Proteins c-akt, Ribosomal Protein S6, TOR Serine-Threonine Kinases.
- chemical , pharmacology : Adenine, Antineoplastic Agents, Phytogenic, Chloroquine, Cisplatin, Sirolimus, Xanthones.
- chemistry : Garcinia.
- drug effects : Autophagy, Cell Proliferation.
- genetics : Autophagy.
- A549 Cells, Cell Line, Tumor, Drug Combinations, Drug Synergism, Gene Expression Regulation, Neoplastic, Humans, Signal Transduction.
Abstract
Gambogic acid (GA) has been shown to inhibit cancer cell proliferation, induce apoptosis, and enhance reactive oxygen species accumulation. However, whether GA could improve multidrug resistance through modulating autophagy has never been explored. We demonstrated that the combination of GA and cisplatin (CDDP) resulted in a stronger growth inhibition effect on A549 and NCI-H460 cells using the MTT assay. Furthermore, treatment with GA significantly increased autophagy in these cells. More importantly, GA-induced cell death could be largely abolished by 3-methyladenine (3-MA) or chloroquine (CQ) treatment, suggesting that GA-induced cell death was dependent on autophagy. Western blot analysis showed that GA treatment suppressed the activation of Akt, mTOR, and S6. In addition, using a GA and rapamycin combination induced more cell death compared to either GA or rapamycin alone. In summary, GA may have utility as an adjunct therapy for non-small cell lung cancer (NSCLC) patients through autophagy-dependent cell death, even when cancer cells have developed resistance to apoptosis.
DOI: 10.1016/j.kjms.2017.06.013
PubMed: 29050671
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pubmed:29050671Le document en format XML
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<term>Gene Expression Regulation, Neoplastic</term>
<term>Humans</term>
<term>Microtubule-Associated Proteins (genetics)</term>
<term>Microtubule-Associated Proteins (metabolism)</term>
<term>Plant Extracts (chemistry)</term>
<term>Proto-Oncogene Proteins c-akt (antagonists & inhibitors)</term>
<term>Proto-Oncogene Proteins c-akt (genetics)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>Ribosomal Protein S6 (antagonists & inhibitors)</term>
<term>Ribosomal Protein S6 (genetics)</term>
<term>Ribosomal Protein S6 (metabolism)</term>
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<term>Protéines proto-oncogènes c-akt</term>
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<term>Protéines proto-oncogènes c-akt</term>
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<term>Sirolimus</term>
<term>Xanthones</term>
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<term>Drug Combinations</term>
<term>Drug Synergism</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>Humans</term>
<term>Signal Transduction</term>
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<term>Autophagie</term>
<term>Cellules A549</term>
<term>Extraits de plantes</term>
<term>Garcinia</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Prolifération cellulaire</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Synergie des médicaments</term>
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<front><div type="abstract" xml:lang="en">Gambogic acid (GA) has been shown to inhibit cancer cell proliferation, induce apoptosis, and enhance reactive oxygen species accumulation. However, whether GA could improve multidrug resistance through modulating autophagy has never been explored. We demonstrated that the combination of GA and cisplatin (CDDP) resulted in a stronger growth inhibition effect on A549 and NCI-H460 cells using the MTT assay. Furthermore, treatment with GA significantly increased autophagy in these cells. More importantly, GA-induced cell death could be largely abolished by 3-methyladenine (3-MA) or chloroquine (CQ) treatment, suggesting that GA-induced cell death was dependent on autophagy. Western blot analysis showed that GA treatment suppressed the activation of Akt, mTOR, and S6. In addition, using a GA and rapamycin combination induced more cell death compared to either GA or rapamycin alone. In summary, GA may have utility as an adjunct therapy for non-small cell lung cancer (NSCLC) patients through autophagy-dependent cell death, even when cancer cells have developed resistance to apoptosis.</div>
</front>
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<DateCompleted><Year>2018</Year>
<Month>06</Month>
<Day>08</Day>
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<DateRevised><Year>2018</Year>
<Month>06</Month>
<Day>08</Day>
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<JournalIssue CitedMedium="Internet"><Volume>33</Volume>
<Issue>11</Issue>
<PubDate><Year>2017</Year>
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<Title>The Kaohsiung journal of medical sciences</Title>
<ISOAbbreviation>Kaohsiung J. Med. Sci.</ISOAbbreviation>
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<ArticleTitle>Gambogic acid improves non-small cell lung cancer progression by inhibition of mTOR signaling pathway.</ArticleTitle>
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<Abstract><AbstractText>Gambogic acid (GA) has been shown to inhibit cancer cell proliferation, induce apoptosis, and enhance reactive oxygen species accumulation. However, whether GA could improve multidrug resistance through modulating autophagy has never been explored. We demonstrated that the combination of GA and cisplatin (CDDP) resulted in a stronger growth inhibition effect on A549 and NCI-H460 cells using the MTT assay. Furthermore, treatment with GA significantly increased autophagy in these cells. More importantly, GA-induced cell death could be largely abolished by 3-methyladenine (3-MA) or chloroquine (CQ) treatment, suggesting that GA-induced cell death was dependent on autophagy. Western blot analysis showed that GA treatment suppressed the activation of Akt, mTOR, and S6. In addition, using a GA and rapamycin combination induced more cell death compared to either GA or rapamycin alone. In summary, GA may have utility as an adjunct therapy for non-small cell lung cancer (NSCLC) patients through autophagy-dependent cell death, even when cancer cells have developed resistance to apoptosis.</AbstractText>
<CopyrightInformation>Copyright © 2017. Published by Elsevier Taiwan.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhao</LastName>
<ForeName>Teng</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, Qilu Hospital of Shandong University, Ji'nan City, Shandong Province, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Hong-Jian</ForeName>
<Initials>HJ</Initials>
<AffiliationInfo><Affiliation>The Second Department of Oncology, Tengzhou Central People's Hospital, Tengzhou City, Shandong Province, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhao</LastName>
<ForeName>Wen-Wen</ForeName>
<Initials>WW</Initials>
<AffiliationInfo><Affiliation>Shandong Maternal and Child Health Care Hospital, Ji'nan City, Shandong Province, PR China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Sun</LastName>
<ForeName>Yi-Ling</ForeName>
<Initials>YL</Initials>
<AffiliationInfo><Affiliation>The Second Department of Oncology, Tengzhou Central People's Hospital, Tengzhou City, Shandong Province, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hu</LastName>
<ForeName>Li-Kuan</ForeName>
<Initials>LK</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, Qilu Hospital of Shandong University, Ji'nan City, Shandong Province, PR China. Electronic address: hulikuan17305@163.com.</Affiliation>
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<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year>
<Month>03</Month>
<Day>08</Day>
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<PubMedPubDate PubStatus="revised"><Year>2017</Year>
<Month>04</Month>
<Day>24</Day>
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<PubMedPubDate PubStatus="accepted"><Year>2017</Year>
<Month>06</Month>
<Day>14</Day>
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<Day>21</Day>
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<PubMedPubDate PubStatus="medline"><Year>2018</Year>
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<Day>9</Day>
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<ArticleId IdType="pii">S1607-551X(17)30149-3</ArticleId>
<ArticleId IdType="doi">10.1016/j.kjms.2017.06.013</ArticleId>
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