دورية أكاديمية
أعرض في EDS

Fasting improves therapeutic response in hepatocellular carcinoma through p53-dependent metabolic synergism.

التفاصيل البيبلوغرافية
العنوان: Fasting improves therapeutic response in hepatocellular carcinoma through p53-dependent metabolic synergism.
المؤلفون: Krstic J; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Cell Biology, Histology and Embryology, Medical University of Graz, 8010 Graz, Austria., Reinisch I; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Cell Biology, Histology and Embryology, Medical University of Graz, 8010 Graz, Austria., Schindlmaier K; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Cell Biology, Histology and Embryology, Medical University of Graz, 8010 Graz, Austria., Galhuber M; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Cell Biology, Histology and Embryology, Medical University of Graz, 8010 Graz, Austria., Riahi Z; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Cell Biology, Histology and Embryology, Medical University of Graz, 8010 Graz, Austria., Berger N; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Cell Biology, Histology and Embryology, Medical University of Graz, 8010 Graz, Austria.; Department of Obstetrics and Gynecology, Medical University of Graz, 8036 Graz, Austria., Kupper N; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Cell Biology, Histology and Embryology, Medical University of Graz, 8010 Graz, Austria., Moyschewitz E; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Cell Biology, Histology and Embryology, Medical University of Graz, 8010 Graz, Austria., Auer M; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Cell Biology, Histology and Embryology, Medical University of Graz, 8010 Graz, Austria., Michenthaler H; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Cell Biology, Histology and Embryology, Medical University of Graz, 8010 Graz, Austria., Nössing C; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Cell Biology, Histology and Embryology, Medical University of Graz, 8010 Graz, Austria.; Cancer Research UK Beatson Institute, Garscube Estate, Glasgow, UK., Depaoli MR; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Molecular Biology and Biochemistry, Medical University of Graz, 8010 Graz, Austria., Ramadani-Muja J; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Molecular Biology and Biochemistry, Medical University of Graz, 8010 Graz, Austria., Usluer S; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Molecular Biology and Biochemistry, Medical University of Graz, 8010 Graz, Austria., Stryeck S; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Molecular Biology and Biochemistry, Medical University of Graz, 8010 Graz, Austria.; Institute of Interactive Systems and Data Science, Graz University of Technology, 8010 Graz, Austria.; Know-Center GmbH, 8010 Graz, Austria., Pichler M; Division of Clinical Oncology, Department of Medicine, Comprehensive Cancer Center Graz, Medical University of Graz, 8036 Graz, Austria., Rinner B; Department for Biomedical Research, Medical University of Graz, Graz, Austria., Deutsch AJA; Division of Hematology, Department of Internal Medicine, Medical University of Graz, 8036 Graz, Austria., Reinisch A; Division of Hematology, Department of Internal Medicine, Medical University of Graz, 8036 Graz, Austria.; Division of Hematology, Department of Blood Group Serology and Transfusion Medicine Medical University of Graz, 8036 Graz, Austria., Madl T; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Molecular Biology and Biochemistry, Medical University of Graz, 8010 Graz, Austria.; BioTechMed-Graz, 8010 Graz, Austria., Chiozzi RZ; Biomolecular Mass Spectrometry and Proteomics, Bijvoet Center for Biomolecular Research and Utrecht Institute of Pharmaceutical Sciences, Utrecht University, 3584CH Utrecht, Netherlands.; Netherlands Proteomics Center, 3584CH Utrecht, Netherlands., Heck AJR; Biomolecular Mass Spectrometry and Proteomics, Bijvoet Center for Biomolecular Research and Utrecht Institute of Pharmaceutical Sciences, Utrecht University, 3584CH Utrecht, Netherlands.; Netherlands Proteomics Center, 3584CH Utrecht, Netherlands., Huch M; Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany., Malli R; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Molecular Biology and Biochemistry, Medical University of Graz, 8010 Graz, Austria.; BioTechMed-Graz, 8010 Graz, Austria., Prokesch A; Gottfried Schatz Research Center for Cell Signaling, Metabolism and Aging, Division of Cell Biology, Histology and Embryology, Medical University of Graz, 8010 Graz, Austria.; BioTechMed-Graz, 8010 Graz, Austria.
المصدر: Science advances [Sci Adv] 2022 Jan 21; Vol. 8 (3), pp. eabh2635. Date of Electronic Publication: 2022 Jan 21.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: American Association for the Advancement of Science Country of Publication: United States NLM ID: 101653440 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2375-2548 (Electronic) Linking ISSN: 23752548 NLM ISO Abbreviation: Sci Adv Subsets: PubMed not MEDLINE; MEDLINE
أسماء مطبوعة: Original Publication: Washington, DC : American Association for the Advancement of Science, [2015]-
مستخلص: Cancer cells voraciously consume nutrients to support their growth, exposing metabolic vulnerabilities that can be therapeutically exploited. Here, we show in hepatocellular carcinoma (HCC) cells, xenografts, and patient-derived organoids that fasting improves sorafenib efficacy and acts synergistically to sensitize sorafenib-resistant HCC. Mechanistically, sorafenib acts noncanonically as an inhibitor of mitochondrial respiration, causing resistant cells to depend on glycolysis for survival. Fasting, through reduction in glucose and impeded AKT/mTOR signaling, prevents this Warburg shift. Regulating glucose transporter and proapoptotic protein expression, p53 is necessary and sufficient for the sorafenib-sensitizing effect of fasting. p53 is also crucial for fasting-mediated improvement of sorafenib efficacy in an orthotopic HCC mouse model. Together, our data suggest fasting and sorafenib as rational combination therapy for HCC with intact p53 signaling. As HCC therapy is currently severely limited by resistance, these results should instigate clinical studies aimed at improving therapy response in advanced-stage HCC.
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معلومات مُعتمدة: W 1226 Austria FWF_ Austrian Science Fund FWF; I 3792 Austria FWF_ Austrian Science Fund FWF; I 3165 Austria FWF_ Austrian Science Fund FWF; DOC 31 Austria FWF_ Austrian Science Fund FWF; P 29328 Austria FWF_ Austrian Science Fund FWF; P 28854 Austria FWF_ Austrian Science Fund FWF; P 34109 Austria FWF_ Austrian Science Fund FWF
تواريخ الأحداث: Date Created: 20220121 Latest Revision: 20240214
رمز التحديث: 20240214
مُعرف محوري في PubMed: PMC8782451
DOI: 10.1126/sciadv.abh2635
PMID: 35061544
قاعدة البيانات: MEDLINE
الوصف
تدمد:2375-2548
DOI:10.1126/sciadv.abh2635