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Anticancer activity of Neosetophomone B by targeting AKT/SKP2/MTH1 axis in leukemic cells.
Kuttikrishnan, Shilpa; Bhat, Ajaz A; Mateo, Jericha M; Ahmad, Fareed; Alali, Feras Q; El-Elimat, Tamam; Oberlies, Nicholas H; Pearce, Cedric J; Uddin, Shahab.
Affiliation
  • Kuttikrishnan S; Translational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar; College of Pharmacy, QU Health, Qatar University, Doha, Qatar.
  • Bhat AA; Laboratory of Molecular and Metabolic Imaging, Cancer Research Department, Sidra Medicine, Doha, Qatar.
  • Mateo JM; Translational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.
  • Ahmad F; Translational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar; Dermatology Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.
  • Alali FQ; College of Pharmacy, QU Health, Qatar University, Doha, Qatar; Biomedical and Pharmaceutical Research Unit, QU Health, Qatar University, Qatar.
  • El-Elimat T; Department of Medicinal Chemistry and Pharmacognosy, Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan.
  • Oberlies NH; Department of Chemistry and Biochemistry, University of North Carolina at Greensboro, Greensboro, NC, 27402, United States.
  • Pearce CJ; Mycosynthetix, Inc., Hillsborough, NC, 27278, United States.
  • Uddin S; Translational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar; Dermatology Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar; Laboratory of Animal Research Center, Qatar University, Doha, Qatar. Electronic address: SKhan34@hamad.qa.
Biochem Biophys Res Commun ; 601: 59-64, 2022 04 23.
Article in En | MEDLINE | ID: mdl-35228122
ABSTRACT
Neosetophomone B (NSP-B), a meroterpenoid fungal secondary metabolite, was investigated for its anticancer potential in leukemic cell lines (K562 and U937). NSP-B treatment of leukemic cells suppressed cell viability by triggering apoptotic cell death. Apoptosis induced by NSP-B is triggered by mitochondrial signaling and caspase activation. Additionally, NSP-B treatment of leukemic cells causes AKT's inactivation accompanied by downregulation of SKP2 oncogene and MTH1 with a concomitant increase of p21Cip1and p27Kip1. Furthermore, NSP-B causes suppression of antiapoptotic proteins, including cIAP1, cIAP2, XIAP, survivin and BCl-XL. Overall, NSP-B reduces cell viability by mitochondrial and caspase-dependent apoptosis. The inhibition of AKT and SKP2 axis could be a promising therapeutic target for leukemia treatment.
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Full text: 1 Collection: 01-internacional Health context: 6_ODS3_enfermedades_notrasmisibles Database: MEDLINE Main subject: Terpenes / Leukemia / Phosphoric Monoester Hydrolases / DNA Repair Enzymes / S-Phase Kinase-Associated Proteins / Proto-Oncogene Proteins c-akt Limits: Humans Language: En Journal: Biochem Biophys Res Commun Year: 2022 Document type: Article
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Full text: 1 Collection: 01-internacional Health context: 6_ODS3_enfermedades_notrasmisibles Database: MEDLINE Main subject: Terpenes / Leukemia / Phosphoric Monoester Hydrolases / DNA Repair Enzymes / S-Phase Kinase-Associated Proteins / Proto-Oncogene Proteins c-akt Limits: Humans Language: En Journal: Biochem Biophys Res Commun Year: 2022 Document type: Article