Feroniellin A-induced autophagy causes apoptosis in multidrug-resistant human A549 lung cancer cells.
Identifieur interne : 000E92 ( Main/Corpus ); précédent : 000E91; suivant : 000E93Feroniellin A-induced autophagy causes apoptosis in multidrug-resistant human A549 lung cancer cells.
Auteurs : Chutima Kaewpiboon ; Serm Surapinit ; Waraporn Malilas ; Jeong Moon ; Preecha Phuwapraisirisan ; Santi Tip-Pyang ; Randal N. Johnston ; Sang Seok Koh ; Wanchai Assavalapsakul ; Young-Hwa ChungSource :
- International journal of oncology [ 1791-2423 ] ; 2014.
English descriptors
- KwdEn :
- ATP Binding Cassette Transporter, Subfamily B (biosynthesis), Antineoplastic Agents (pharmacology), Apoptosis (drug effects), Apoptosis (genetics), Apoptosis Regulatory Proteins (genetics), Autophagy (drug effects), Beclin-1 (MeSH), Cell Line, Tumor (MeSH), Coumarins (pharmacology), Drug Resistance, Neoplasm (drug effects), Etoposide (pharmacology), Furans (pharmacology), Glycosides (pharmacology), Humans (MeSH), Lung Neoplasms (drug therapy), Membrane Proteins (genetics), Microfilament Proteins (MeSH), Nitriles (pharmacology), Promoter Regions, Genetic (MeSH), RNA Interference (MeSH), RNA, Small Interfering (MeSH), Sirolimus (pharmacology), Sulfones (pharmacology), Transcription Factor RelA (antagonists & inhibitors), Transcription Factor RelA (biosynthesis), Transcription, Genetic (MeSH).
- MESH :
- chemical , antagonists & inhibitors : Transcription Factor RelA.
- chemical , biosynthesis : ATP Binding Cassette Transporter, Subfamily B, Transcription Factor RelA.
- chemical , genetics : Apoptosis Regulatory Proteins, Membrane Proteins.
- chemical , pharmacology : Antineoplastic Agents, Coumarins, Etoposide, Furans, Glycosides, Nitriles, Sirolimus, Sulfones.
- drug effects : Apoptosis, Autophagy, Drug Resistance, Neoplasm.
- drug therapy : Lung Neoplasms.
- genetics : Apoptosis.
- chemical : Beclin-1, Cell Line, Tumor, Humans, Microfilament Proteins, Promoter Regions, Genetic, RNA Interference, RNA, Small Interfering, Transcription, Genetic.
Abstract
During the screening of natural chemicals that can reverse multidrug resistance in human A549 lung cancer cells resistant to etoposide (A549RT-eto), we discovered that Feroniellin A (FERO), a novel furanocoumarin, shows toxicity toward A549RT-eto cells in a dose- and time-dependent manner. FERO reduced the expression of NF-κB, leading to downregulation of P-glycoprotein (P-gp), encoded by MDR1, which eventually sensitized A549RT-eto cells to apoptosis. FERO specifically diminished transcription and promoter activity of MDR1 but did not inhibit the expression of other multidrug resistance genes MRP2 and BCRP. Moreover, co-administration of FERO with Bay11-7802, an inhibitor of NF-κB, accelerated apoptosis of A549RT-eto cells through decreased expression of P-gp, indicating that NF-κB is involved in multidrug resistance. Conversely, addition of Z-VAD, a pan-caspase inhibitor, blocked FERO-induced apoptosis in A549RT-eto cells but did not block downregulation of P-gp, indicating that a decrease in P-gp expression is necessary but not sufficient for FERO-induced apoptosis. Interestingly, we found that FERO also induces autophagy, which is characterized by the conversion of LC3 I to LC3 II, induction of GFP-LC3 puncta, enhanced expression of Beclin-1 and ATG5, and inactivation of mTOR. Furthermore, suppression of Beclin-1 by siRNA reduced FERO-induced apoptosis in A549RT-eto cells and activation of autophagy by rapamycin accelerated FERO-induced apoptosis, suggesting that autophagy plays an active role in FERO-induced apoptosis. Herein, we report that FERO reverses multidrug resistance in A549RT-eto cells and exerts its cytotoxic effect by induction of both autophagy and apoptosis, which suggests that FERO can be a useful anticancer drug for multidrug-resistant lung cancer.
DOI: 10.3892/ijo.2014.2297
PubMed: 24535083
Links to Exploration step
pubmed:24535083Le document en format XML
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<term>Apoptosis (genetics)</term>
<term>Apoptosis Regulatory Proteins (genetics)</term>
<term>Autophagy (drug effects)</term>
<term>Beclin-1 (MeSH)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Coumarins (pharmacology)</term>
<term>Drug Resistance, Neoplasm (drug effects)</term>
<term>Etoposide (pharmacology)</term>
<term>Furans (pharmacology)</term>
<term>Glycosides (pharmacology)</term>
<term>Humans (MeSH)</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Membrane Proteins (genetics)</term>
<term>Microfilament Proteins (MeSH)</term>
<term>Nitriles (pharmacology)</term>
<term>Promoter Regions, Genetic (MeSH)</term>
<term>RNA Interference (MeSH)</term>
<term>RNA, Small Interfering (MeSH)</term>
<term>Sirolimus (pharmacology)</term>
<term>Sulfones (pharmacology)</term>
<term>Transcription Factor RelA (antagonists & inhibitors)</term>
<term>Transcription Factor RelA (biosynthesis)</term>
<term>Transcription, Genetic (MeSH)</term>
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<term>Membrane Proteins</term>
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<term>Etoposide</term>
<term>Furans</term>
<term>Glycosides</term>
<term>Nitriles</term>
<term>Sirolimus</term>
<term>Sulfones</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
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<term>Humans</term>
<term>Microfilament Proteins</term>
<term>Promoter Regions, Genetic</term>
<term>RNA Interference</term>
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<front><div type="abstract" xml:lang="en">During the screening of natural chemicals that can reverse multidrug resistance in human A549 lung cancer cells resistant to etoposide (A549RT-eto), we discovered that Feroniellin A (FERO), a novel furanocoumarin, shows toxicity toward A549RT-eto cells in a dose- and time-dependent manner. FERO reduced the expression of NF-κB, leading to downregulation of P-glycoprotein (P-gp), encoded by MDR1, which eventually sensitized A549RT-eto cells to apoptosis. FERO specifically diminished transcription and promoter activity of MDR1 but did not inhibit the expression of other multidrug resistance genes MRP2 and BCRP. Moreover, co-administration of FERO with Bay11-7802, an inhibitor of NF-κB, accelerated apoptosis of A549RT-eto cells through decreased expression of P-gp, indicating that NF-κB is involved in multidrug resistance. Conversely, addition of Z-VAD, a pan-caspase inhibitor, blocked FERO-induced apoptosis in A549RT-eto cells but did not block downregulation of P-gp, indicating that a decrease in P-gp expression is necessary but not sufficient for FERO-induced apoptosis. Interestingly, we found that FERO also induces autophagy, which is characterized by the conversion of LC3 I to LC3 II, induction of GFP-LC3 puncta, enhanced expression of Beclin-1 and ATG5, and inactivation of mTOR. Furthermore, suppression of Beclin-1 by siRNA reduced FERO-induced apoptosis in A549RT-eto cells and activation of autophagy by rapamycin accelerated FERO-induced apoptosis, suggesting that autophagy plays an active role in FERO-induced apoptosis. Herein, we report that FERO reverses multidrug resistance in A549RT-eto cells and exerts its cytotoxic effect by induction of both autophagy and apoptosis, which suggests that FERO can be a useful anticancer drug for multidrug-resistant lung cancer.</div>
</front>
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<Month>11</Month>
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<DateRevised><Year>2018</Year>
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<Title>International journal of oncology</Title>
<ISOAbbreviation>Int J Oncol</ISOAbbreviation>
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<ArticleTitle>Feroniellin A-induced autophagy causes apoptosis in multidrug-resistant human A549 lung cancer cells.</ArticleTitle>
<Pagination><MedlinePgn>1233-42</MedlinePgn>
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<ELocationID EIdType="doi" ValidYN="Y">10.3892/ijo.2014.2297</ELocationID>
<Abstract><AbstractText>During the screening of natural chemicals that can reverse multidrug resistance in human A549 lung cancer cells resistant to etoposide (A549RT-eto), we discovered that Feroniellin A (FERO), a novel furanocoumarin, shows toxicity toward A549RT-eto cells in a dose- and time-dependent manner. FERO reduced the expression of NF-κB, leading to downregulation of P-glycoprotein (P-gp), encoded by MDR1, which eventually sensitized A549RT-eto cells to apoptosis. FERO specifically diminished transcription and promoter activity of MDR1 but did not inhibit the expression of other multidrug resistance genes MRP2 and BCRP. Moreover, co-administration of FERO with Bay11-7802, an inhibitor of NF-κB, accelerated apoptosis of A549RT-eto cells through decreased expression of P-gp, indicating that NF-κB is involved in multidrug resistance. Conversely, addition of Z-VAD, a pan-caspase inhibitor, blocked FERO-induced apoptosis in A549RT-eto cells but did not block downregulation of P-gp, indicating that a decrease in P-gp expression is necessary but not sufficient for FERO-induced apoptosis. Interestingly, we found that FERO also induces autophagy, which is characterized by the conversion of LC3 I to LC3 II, induction of GFP-LC3 puncta, enhanced expression of Beclin-1 and ATG5, and inactivation of mTOR. Furthermore, suppression of Beclin-1 by siRNA reduced FERO-induced apoptosis in A549RT-eto cells and activation of autophagy by rapamycin accelerated FERO-induced apoptosis, suggesting that autophagy plays an active role in FERO-induced apoptosis. Herein, we report that FERO reverses multidrug resistance in A549RT-eto cells and exerts its cytotoxic effect by induction of both autophagy and apoptosis, which suggests that FERO can be a useful anticancer drug for multidrug-resistant lung cancer.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kaewpiboon</LastName>
<ForeName>Chutima</ForeName>
<Initials>C</Initials>
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<MeshHeading><DescriptorName UI="D019008" MajorTopicYN="N">Drug Resistance, Neoplasm</DescriptorName>
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<MeshHeading><DescriptorName UI="D005663" MajorTopicYN="N">Furans</DescriptorName>
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<MeshHeading><DescriptorName UI="D006027" MajorTopicYN="N">Glycosides</DescriptorName>
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<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
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<MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName>
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<MeshHeading><DescriptorName UI="D008565" MajorTopicYN="N">Membrane Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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<MeshHeading><DescriptorName UI="D008840" MajorTopicYN="N">Microfilament Proteins</DescriptorName>
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<MeshHeading><DescriptorName UI="D009570" MajorTopicYN="N">Nitriles</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
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<MeshHeading><DescriptorName UI="D011401" MajorTopicYN="N">Promoter Regions, Genetic</DescriptorName>
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<MeshHeading><DescriptorName UI="D034622" MajorTopicYN="N">RNA Interference</DescriptorName>
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<MeshHeading><DescriptorName UI="D034741" MajorTopicYN="N">RNA, Small Interfering</DescriptorName>
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<MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName>
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<MeshHeading><DescriptorName UI="D013450" MajorTopicYN="N">Sulfones</DescriptorName>
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<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year>
<Month>11</Month>
<Day>27</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2014</Year>
<Month>01</Month>
<Day>30</Day>
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<PubMedPubDate PubStatus="entrez"><Year>2014</Year>
<Month>2</Month>
<Day>19</Day>
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<Day>19</Day>
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<PubMedPubDate PubStatus="medline"><Year>2014</Year>
<Month>12</Month>
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<ArticleIdList><ArticleId IdType="pubmed">24535083</ArticleId>
<ArticleId IdType="doi">10.3892/ijo.2014.2297</ArticleId>
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