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Vitamin D Modulation of Mitochondrial Oxidative Metabolism and mTOR Enforces Stress Adaptations and Anticancer Responses.

التفاصيل البيبلوغرافية
العنوان: Vitamin D Modulation of Mitochondrial Oxidative Metabolism and mTOR Enforces Stress Adaptations and Anticancer Responses.
المؤلفون: Quigley M; Biology Department University of Miami Coral Gables FL USA.; Dana Farber Cancer Institute Boston MA USA., Rieger S; Biology Department University of Miami Coral Gables FL USA.; Sylvester Comprehensive Cancer Center, Miller School of Medicine University of Miami Miami FL USA., Capobianco E; Institute for Data Science and Computing University of Miami Coral Gables FL USA., Wang Z; Department of Computer Science University of Miami Coral Gables FL USA., Zhao H; Department of Dermatology The First Affiliated Hospital of Chongqing Medical University Chongqing China., Hewison M; Institute of Metabolism and Systems Research University of Birmingham Birmingham UK., Lisse TS; Biology Department University of Miami Coral Gables FL USA.; Sylvester Comprehensive Cancer Center, Miller School of Medicine University of Miami Miami FL USA.
المصدر: JBMR plus [JBMR Plus] 2021 Dec 01; Vol. 6 (1), pp. e10572. Date of Electronic Publication: 2021 Dec 01 (Print Publication: 2022).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Oxford University Press Country of Publication: England NLM ID: 101707013 Publication Model: eCollection Cited Medium: Internet ISSN: 2473-4039 (Electronic) Linking ISSN: 24734039 NLM ISO Abbreviation: JBMR Plus Subsets: PubMed not MEDLINE
أسماء مطبوعة: Publication: 2024- : Oxford : Oxford University Press
Original Publication: [Chichester, West Sussex, UK] : John Wiley & Sons, [2017]-
مستخلص: The relationship between the active form of vitamin D 3 (1,25-dihydroxyvitamin D, 1,25(OH) 2 D) and reactive oxygen species (ROS), two integral signaling molecules of the cell, is poorly understood. This is striking, given that both factors are involved in cancer cell regulation and metabolism. Mitochondria (mt) dysfunction is one of the main drivers of cancer, producing more mitochondria, higher cellular energy, and ROS that can enhance oxidative stress and stress tolerance responses. To study the effects of 1,25(OH) 2 D on metabolic and mt dysfunction, we used the vitamin D receptor (VDR)-sensitive MG-63 osteosarcoma cell model. Using biochemical approaches, 1,25(OH) 2 D decreased mt ROS levels, membrane potential (ΔΨ mt ), biogenesis, and translation, while enforcing endoplasmic reticulum/mitohormetic stress adaptive responses. Using a mitochondria-focused transcriptomic approach, gene set enrichment and pathway analyses show that 1,25(OH) 2 D lowered mt fusion/fission and oxidative phosphorylation (OXPHOS). By contrast, mitophagy, ROS defense, and epigenetic gene regulation were enhanced after 1,25(OH) 2 D treatment, as well as key metabolic enzymes that regulate fluxes of substrates for cellular architecture and a shift toward non-oxidative energy metabolism. ATACseq revealed putative oxi-sensitive and tumor-suppressing transcription factors that may regulate important mt functional genes such as the mTORC1 inhibitor, DDIT4/REDD1 . DDIT4/REDD1 was predominantly localized to the outer mt membrane in untreated MG-63 cells yet sequestered in the cytoplasm after 1,25(OH) 2 D and rotenone treatments, suggesting a level of control by membrane depolarization to facilitate its cytoplasmic mTORC1 inhibitory function. The results show that 1,25(OH) 2 D activates distinct adaptive metabolic responses involving mitochondria to regain redox balance and control the growth of osteosarcoma cells. © 2021 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.
(© 2021 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.)
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معلومات مُعتمدة: R01 CA215973 United States CA NCI NIH HHS
فهرسة مساهمة: Keywords: BONE; CANCER; CYP24A1; DDIT4; METABOLISM; MG‐63; MITOCHONDRIA; OSTEOBLAST; OSTEOSARCOMA; REDD1; ROS; SOD; SOD1; SOD2; STRESS; TUMOR; UNFOLDED PROTEIN RESPONSE; VDR; VITAMIN D; VITAMIN D DEFICIENCY; VITAMIN D RECEPTOR
تواريخ الأحداث: Date Created: 20220126 Latest Revision: 20240510
رمز التحديث: 20240510
مُعرف محوري في PubMed: PMC8771003
DOI: 10.1002/jbm4.10572
PMID: 35079680
قاعدة البيانات: MEDLINE
الوصف
تدمد:2473-4039
DOI:10.1002/jbm4.10572