FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1489805896> ?p ?o ?g. }

• W1489805896 endingPage "1530" @default.
• W1489805896 startingPage "1519" @default.
• W1489805896 abstract "// Chuan Bian Lim 1 , Cecilia M. Prêle 1, 2 , Svetlana Baltic 1 , Peter G. Arthur 3 , Jenette Creaney 4 , D. Neil Watkins 5 , Philip J. Thompson 1 , Steven E. Mutsaers 1, 2 1 Lung Institute of Western Australia and Centre for Asthma, Allergy and Respiratory Research, School of Medicine and Pharmacology, University of Western Australia, Harry Perkins Institute of Medical Research, Nedlands, WA, Australia 2 Centre for Cell Therapy and Regenerative Medicine, School of Medicine and Pharmacology, University of Western Australia and Harry Perkins Institute of Medical Research, Nedlands, WA, Australia 3 School of Chemistry and Biochemistry, University of Western Australia, Crawley, WA, Australia 4 National Centre for Asbestos Related Diseases, School of Medicine and Pharmacology, University of Western Australia, Harry Perkins Institute of Medical Research and Australian Mesothelioma Tissue Bank, Sir Charles Gairdner Hospital, Nedlands, WA, Australia 5 Garvan Institute of Medical Research, Darlinghurst, NSW, Australia Correspondence to: Steven E. Mutsaers, e-mail: mutsaers@liwa.uwa.edu.au Keywords: Apoptosis, mesothelioma, GANT61, Hedgehog, reactive oxygen species Received: September 02, 2014      Accepted: November 08, 2014      Published: January 03, 2015 ABSTRACT Gli transcription factors of the Hedgehog (Hh) pathway have been reported to be drivers of malignant mesothelioma (MMe) cell survival. The Gli inhibitor GANT61 induces apoptosis in various cancer cell models, and has been associated directly with Gli inhibition. However various chemotherapeutics can induce cell death through generation of reactive oxygen species (ROS) but whether ROS mediates GANT61-induced apoptosis is unknown. In this study human MMe cells were treated with GANT61 and the mechanisms regulating cell death investigated. Exposure of MMe cells to GANT61 led to G1 phase arrest and apoptosis, which involved ROS but not its purported targets, GLI1 or GLI2. GANT61 triggered ROS generation and quenching of ROS protected MMe cells from GANT61-induced apoptosis. Furthermore, we demonstrated that mitochondria are important in mediating GANT61 effects: (1) ROS production and apoptosis were blocked by mitochondrial inhibitor rotenone; (2) GANT61 promoted superoxide formation in mitochondria; and (3) mitochondrial DNA-deficient LO68 cells failed to induce superoxide, and were more resistant to apoptosis induced by GANT61 than wild-type cells. Our data demonstrate for the first time that GANT61 induces apoptosis by promoting mitochondrial superoxide generation independent of Gli inhibition, and highlights the therapeutic potential of mitochondrial ROS-mediated anticancer drugs in MMe." @default.
• W1489805896 created "2016-06-24" @default.
• W1489805896 creator A5013062013 @default.
• W1489805896 creator A5020706368 @default.
• W1489805896 creator A5029837255 @default.
• W1489805896 creator A5032038986 @default.
• W1489805896 creator A5042431804 @default.
• W1489805896 creator A5051279706 @default.
• W1489805896 creator A5069849291 @default.
• W1489805896 creator A5089712853 @default.
• W1489805896 date "2015-01-16" @default.
• W1489805896 modified "2023-10-16" @default.
• W1489805896 title "Mitochondria-derived reactive oxygen species drive GANT61-induced mesothelioma cell apoptosis" @default.
• W1489805896 cites W1569836364 @default.
• W1489805896 cites W1974090542 @default.
• W1489805896 cites W1975217692 @default.
• W1489805896 cites W1978626648 @default.
• W1489805896 cites W1981286174 @default.
• W1489805896 cites W1993416164 @default.
• W1489805896 cites W1994620081 @default.
• W1489805896 cites W1998343230 @default.
• W1489805896 cites W2000718634 @default.
• W1489805896 cites W2009286988 @default.
• W1489805896 cites W2017275974 @default.
• W1489805896 cites W2029431452 @default.
• W1489805896 cites W2054657634 @default.
• W1489805896 cites W2054863805 @default.
• W1489805896 cites W2060893987 @default.
• W1489805896 cites W2069912181 @default.
• W1489805896 cites W2070920469 @default.
• W1489805896 cites W2071463209 @default.
• W1489805896 cites W2075387097 @default.
• W1489805896 cites W2080823574 @default.
• W1489805896 cites W2083169077 @default.
• W1489805896 cites W2089179512 @default.
• W1489805896 cites W2097299991 @default.
• W1489805896 cites W2100562940 @default.
• W1489805896 cites W2108707301 @default.
• W1489805896 cites W2110321605 @default.
• W1489805896 cites W2125475436 @default.
• W1489805896 cites W2126411666 @default.
• W1489805896 cites W2127428044 @default.
• W1489805896 cites W2131561057 @default.
• W1489805896 cites W2138270921 @default.
• W1489805896 cites W2139607880 @default.
• W1489805896 cites W2141178172 @default.
• W1489805896 cites W2144104511 @default.
• W1489805896 cites W2146738245 @default.
• W1489805896 cites W2151907359 @default.
• W1489805896 cites W2163036693 @default.
• W1489805896 cites W2167340008 @default.
• W1489805896 cites W4254119740 @default.
• W1489805896 cites W4362172418 @default.
• W1489805896 doi "https://doi.org/10.18632/oncotarget.2729" @default.
• W1489805896 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4359311" @default.
• W1489805896 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25544756" @default.
• W1489805896 hasPublicationYear "2015" @default.
• W1489805896 type Work @default.
• W1489805896 sameAs 1489805896 @default.
• W1489805896 citedByCount "25" @default.
• W1489805896 countsByYear W14898058962015 @default.
• W1489805896 countsByYear W14898058962016 @default.
• W1489805896 countsByYear W14898058962017 @default.
• W1489805896 countsByYear W14898058962018 @default.
• W1489805896 countsByYear W14898058962019 @default.
• W1489805896 countsByYear W14898058962020 @default.
• W1489805896 countsByYear W14898058962022 @default.
• W1489805896 crossrefType "journal-article" @default.
• W1489805896 hasAuthorship W1489805896A5013062013 @default.
• W1489805896 hasAuthorship W1489805896A5020706368 @default.
• W1489805896 hasAuthorship W1489805896A5029837255 @default.
• W1489805896 hasAuthorship W1489805896A5032038986 @default.
• W1489805896 hasAuthorship W1489805896A5042431804 @default.
• W1489805896 hasAuthorship W1489805896A5051279706 @default.
• W1489805896 hasAuthorship W1489805896A5069849291 @default.
• W1489805896 hasAuthorship W1489805896A5089712853 @default.
• W1489805896 hasBestOaLocation W14898058961 @default.
• W1489805896 hasConcept C142724271 @default.
• W1489805896 hasConcept C185592680 @default.
• W1489805896 hasConcept C190283241 @default.
• W1489805896 hasConcept C2777407522 @default.
• W1489805896 hasConcept C2778539099 @default.
• W1489805896 hasConcept C48349386 @default.
• W1489805896 hasConcept C502942594 @default.
• W1489805896 hasConcept C55493867 @default.
• W1489805896 hasConcept C62478195 @default.
• W1489805896 hasConcept C71924100 @default.
• W1489805896 hasConceptScore W1489805896C142724271 @default.
• W1489805896 hasConceptScore W1489805896C185592680 @default.
• W1489805896 hasConceptScore W1489805896C190283241 @default.
• W1489805896 hasConceptScore W1489805896C2777407522 @default.
• W1489805896 hasConceptScore W1489805896C2778539099 @default.
• W1489805896 hasConceptScore W1489805896C48349386 @default.
• W1489805896 hasConceptScore W1489805896C502942594 @default.
• W1489805896 hasConceptScore W1489805896C55493867 @default.
• W1489805896 hasConceptScore W1489805896C62478195 @default.
• W1489805896 hasConceptScore W1489805896C71924100 @default.
• W1489805896 hasIssue "3" @default.

• next