Autophagy flux inhibition mediated by celastrol sensitized lung cancer cells to TRAIL‑induced apoptosis via regulation of mitochondrial transmembrane potential and reactive oxygen species.
Identifieur interne : 000064 ( PubMed/Checkpoint ); précédent : 000063; suivant : 000065Autophagy flux inhibition mediated by celastrol sensitized lung cancer cells to TRAIL‑induced apoptosis via regulation of mitochondrial transmembrane potential and reactive oxygen species.
Auteurs : Uddin Md Nazim [Corée du Sud] ; Honghua Yin [Corée du Sud] ; Sang-Youel Park [Corée du Sud]Source :
- Molecular medicine reports [ 1791-3004 ] ; 2019.
Descripteurs français
- KwdFr :
- Acétylcystéine (pharmacologie), Antinéoplasiques d'origine végétale (antagonistes et inhibiteurs), Antinéoplasiques d'origine végétale (pharmacologie), Apoptose (), Apoptose (génétique), Association médicamenteuse, Autophagie (), Autophagie (génétique), Caspase 8 (génétique), Caspase 8 (métabolisme), Cellules A549, Chloroquine (pharmacologie), Espèces réactives de l'oxygène (agonistes), Espèces réactives de l'oxygène (métabolisme), Humains, Ligand TRAIL (pharmacologie), Lignée cellulaire tumorale, Mitochondries (), Mitochondries (métabolisme), Potentiel de membrane mitochondriale (), Protéines associées aux microtubules (génétique), Protéines associées aux microtubules (métabolisme), Régulation de l'expression des gènes tumoraux, Synergie des médicaments, Séquestosome-1 (génétique), Séquestosome-1 (métabolisme), Transduction du signal, Triterpènes (antagonistes et inhibiteurs), Triterpènes (pharmacologie).
- MESH :
- agonistes : Espèces réactives de l'oxygène.
- antagonistes et inhibiteurs : Antinéoplasiques d'origine végétale, Triterpènes.
- génétique : Apoptose, Autophagie, Caspase 8, Protéines associées aux microtubules, Séquestosome-1.
- métabolisme : Caspase 8, Espèces réactives de l'oxygène, Mitochondries, Protéines associées aux microtubules, Séquestosome-1.
- pharmacologie : Acétylcystéine, Antinéoplasiques d'origine végétale, Chloroquine, Ligand TRAIL, Triterpènes.
- Apoptose, Association médicamenteuse, Autophagie, Cellules A549, Humains, Lignée cellulaire tumorale, Mitochondries, Potentiel de membrane mitochondriale, Régulation de l'expression des gènes tumoraux, Synergie des médicaments, Transduction du signal.
English descriptors
- KwdEn :
- A549 Cells, Acetylcysteine (pharmacology), Antineoplastic Agents, Phytogenic (antagonists & inhibitors), Antineoplastic Agents, Phytogenic (pharmacology), Apoptosis (drug effects), Apoptosis (genetics), Autophagy (drug effects), Autophagy (genetics), Caspase 8 (genetics), Caspase 8 (metabolism), Cell Line, Tumor, Chloroquine (pharmacology), Drug Combinations, Drug Synergism, Gene Expression Regulation, Neoplastic, Humans, Membrane Potential, Mitochondrial (drug effects), Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (metabolism), Mitochondria (drug effects), Mitochondria (metabolism), Reactive Oxygen Species (agonists), Reactive Oxygen Species (metabolism), Sequestosome-1 Protein (genetics), Sequestosome-1 Protein (metabolism), Signal Transduction, TNF-Related Apoptosis-Inducing Ligand (pharmacology), Triterpenes (antagonists & inhibitors), Triterpenes (pharmacology).
- MESH :
- chemical , agonists : Reactive Oxygen Species.
- chemical , antagonists & inhibitors : Antineoplastic Agents, Phytogenic, Triterpenes.
- chemical , genetics : Caspase 8, Microtubule-Associated Proteins, Sequestosome-1 Protein.
- chemical , metabolism : Caspase 8, Microtubule-Associated Proteins, Reactive Oxygen Species, Sequestosome-1 Protein.
- chemical , pharmacology : Acetylcysteine, Antineoplastic Agents, Phytogenic, Chloroquine, TNF-Related Apoptosis-Inducing Ligand, Triterpenes.
- drug effects : Apoptosis, Autophagy, Membrane Potential, Mitochondrial, Mitochondria.
- genetics : Apoptosis, Autophagy.
- metabolism : Mitochondria.
- A549 Cells, Cell Line, Tumor, Drug Combinations, Drug Synergism, Gene Expression Regulation, Neoplastic, Humans, Signal Transduction.
Abstract
Tumor necrosis factor‑related apoptosis-inducing ligand (TRAIL) is well known as a transmembrane cytokine and has been proposed as one of the most effective anti‑cancer therapeutic agents, owing to its efficiency to selectively induce cell death in a variety of tumor cells. Suppression of autophagy flux has been increasingly acknowledged as an effective and novel therapeutic intervention for cancer. The present study demonstrated that the anti‑cancer and anti‑inflammatory drug celastrol, through its anti‑metastatic properties, may initiate TRAIL‑mediated apoptotic cell death in lung cancer cells. This sensitization was negatively affected by N‑acetyl‑l‑cysteine, which restored the mitochondrial membrane potential (ΔΨm) and inhibited reactive oxygen species (ROS) generation. Notably, treatment with celastrol caused an increase in microtubule‑associated proteins 1A/1B light chain 3B‑II and p62 levels, whereas co‑treatment of celastrol and TRAIL increased active caspase 3 and 8 levels compared with the control, confirming inhibited autophagy flux. The combined use of TRAIL with celastrol may serve as a safe and adequate therapeutic technique for the treatment of TRAIL‑resistant lung cancer, suggesting that celastrol‑mediated autophagy flux inhibition sensitized TRAIL‑initiated apoptosis via regulation of ROS and ΔΨm.
DOI: 10.3892/mmr.2018.9757
PubMed: 30569150
Affiliations:
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signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Tumor necrosis factor‑related apoptosis-inducing ligand (TRAIL) is well known as a transmembrane cytokine and has been proposed as one of the most effective anti‑cancer therapeutic agents, owing to its efficiency to selectively induce cell death in a variety of tumor cells. Suppression of autophagy flux has been increasingly acknowledged as an effective and novel therapeutic intervention for cancer. The present study demonstrated that the anti‑cancer and anti‑inflammatory drug celastrol, through its anti‑metastatic properties, may initiate TRAIL‑mediated apoptotic cell death in lung cancer cells. This sensitization was negatively affected by N‑acetyl‑l‑cysteine, which restored the mitochondrial membrane potential (ΔΨm) and inhibited reactive oxygen species (ROS) generation. Notably, treatment with celastrol caused an increase in microtubule‑associated proteins 1A/1B light chain 3B‑II and p62 levels, whereas co‑treatment of celastrol and TRAIL increased active caspase 3 and 8 levels compared with the control, confirming inhibited autophagy flux. The combined use of TRAIL with celastrol may serve as a safe and adequate therapeutic technique for the treatment of TRAIL‑resistant lung cancer, suggesting that celastrol‑mediated autophagy flux inhibition sensitized TRAIL‑initiated apoptosis via regulation of ROS and ΔΨm.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30569150</PMID><DateCompleted><Year>2019</Year><Month>05</Month><Day>24</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1791-3004</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><Issue>2</Issue><PubDate><Year>2019</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Molecular medicine reports</Title><ISOAbbreviation>Mol Med Rep</ISOAbbreviation></Journal><ArticleTitle>Autophagy flux inhibition mediated by celastrol sensitized lung cancer cells to TRAIL‑induced apoptosis via regulation of mitochondrial transmembrane potential and reactive oxygen species.</ArticleTitle><Pagination><MedlinePgn>984-993</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3892/mmr.2018.9757</ELocationID><Abstract><AbstractText>Tumor necrosis factor‑related apoptosis-inducing ligand (TRAIL) is well known as a transmembrane cytokine and has been proposed as one of the most effective anti‑cancer therapeutic agents, owing to its efficiency to selectively induce cell death in a variety of tumor cells. Suppression of autophagy flux has been increasingly acknowledged as an effective and novel therapeutic intervention for cancer. The present study demonstrated that the anti‑cancer and anti‑inflammatory drug celastrol, through its anti‑metastatic properties, may initiate TRAIL‑mediated apoptotic cell death in lung cancer cells. This sensitization was negatively affected by N‑acetyl‑l‑cysteine, which restored the mitochondrial membrane potential (ΔΨm) and inhibited reactive oxygen species (ROS) generation. Notably, treatment with celastrol caused an increase in microtubule‑associated proteins 1A/1B light chain 3B‑II and p62 levels, whereas co‑treatment of celastrol and TRAIL increased active caspase 3 and 8 levels compared with the control, confirming inhibited autophagy flux. The combined use of TRAIL with celastrol may serve as a safe and adequate therapeutic technique for the treatment of TRAIL‑resistant lung cancer, suggesting that celastrol‑mediated autophagy flux inhibition sensitized TRAIL‑initiated apoptosis via regulation of ROS and ΔΨm.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nazim</LastName><ForeName>Uddin Md</ForeName><Initials>UM</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, Jeonbuk 54596, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yin</LastName><ForeName>Honghua</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, Jeonbuk 54596, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Sang-Youel</ForeName><Initials>SY</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, Jeonbuk 54596, Republic of Korea.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>12</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>Greece</Country><MedlineTA>Mol Med Rep</MedlineTA><NlmUniqueID>101475259</NlmUniqueID><ISSNLinking>1791-2997</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000972">Antineoplastic Agents, Phytogenic</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004338">Drug Combinations</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C502070">MAP1LC3B protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008869">Microtubule-Associated Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C099718">SQSTM1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000071456">Sequestosome-1 Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053221">TNF-Related Apoptosis-Inducing Ligand</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C505653">TNFSF10 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014315">Triterpenes</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="C505530">CASP8 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.22.-</RegistryNumber><NameOfSubstance UI="D053181">Caspase 8</NameOfSubstance></Chemical><Chemical><RegistryNumber>L8GG98663L</RegistryNumber><NameOfSubstance UI="C050414">tripterine</NameOfSubstance></Chemical><Chemical><RegistryNumber>WYQ7N0BPYC</RegistryNumber><NameOfSubstance UI="D000111">Acetylcysteine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000072283" MajorTopicYN="N">A549 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000111" MajorTopicYN="N">Acetylcysteine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000972" MajorTopicYN="N">Antineoplastic Agents, Phytogenic</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053181" MajorTopicYN="N">Caspase 8</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</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="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004338" MajorTopicYN="N">Drug Combinations</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004357" MajorTopicYN="N">Drug Synergism</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015972" MajorTopicYN="Y">Gene Expression Regulation, Neoplastic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053078" MajorTopicYN="N">Membrane Potential, Mitochondrial</DescriptorName><QualifierName UI="Q000187" 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