Vitamin E succinate mediated apoptosis by juxtaposing endoplasmic reticulum and mitochondria
Vitamin E succinate (VES) is an esterified form of natural α-tocopherol, has turned out to be novel anticancer agent. However, its anticancer mechanisms have not been illustrated. Previously, we reported VES mediated Ca2+ release from the endoplasmic reticulum (ER) causes mitochondrial Ca2+ overload...
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| Published in | Biochimica et biophysica acta. General subjects Vol. 1867; no. 12; p. 130485 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
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01.12.2023
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| Abstract | Vitamin E succinate (VES) is an esterified form of natural α-tocopherol, has turned out to be novel anticancer agent. However, its anticancer mechanisms have not been illustrated. Previously, we reported VES mediated Ca2+ release from the endoplasmic reticulum (ER) causes mitochondrial Ca2+ overload, leading to mitochondrial depolarization and apoptosis. Here, we elucidated the mechanism of VES-induced Ca2+ transfer from ER to mitochondria by investigating the role of VES in ER-mitochondria contact formation. Transmission electron microscopic observation confirms VES mediated ER-mitochondria contact while fluorescence microscopic analysis revealed that VES increased mitochondria-associated ER membrane (MAM) formation. Pre-treatment with the inositol 1,4,5-triphosphate receptor (IP3R) antagonist 2-aminoethyl diphenylborinate (2-APB) decreased VES-induced MAM formation, suggesting the involvement of VES-induced Ca2+ efflux from ER in MAM formation. The ER IP3R receptor is known to interact with voltage-dependent anion channels (VDAC) via the chaperone glucose-regulated protein 75 kDa (GRP75) to bring ER and mitochondria nearby. Although we revealed that VES treatment does not affect GRP75 protein level, it increases GRP75 localization in the MAM. In addition, the inhibition of Ca2+ release from ER by 2-APB decreases GRP75 localization in the MAM, suggesting the possibility of Ca2+-induced conformational change of GRP75 that promotes formation of the IP3R-GRP75-VDAC complex and thereby encourages MAM formation. This study identifies the mechanism of VES-induced enhanced Ca2+ transfer from ER to mitochondria, which causes mitochondrial Ca2+ overload leading to apoptosis.Vitamin E succinate (VES) is an esterified form of natural α-tocopherol, has turned out to be novel anticancer agent. However, its anticancer mechanisms have not been illustrated. Previously, we reported VES mediated Ca2+ release from the endoplasmic reticulum (ER) causes mitochondrial Ca2+ overload, leading to mitochondrial depolarization and apoptosis. Here, we elucidated the mechanism of VES-induced Ca2+ transfer from ER to mitochondria by investigating the role of VES in ER-mitochondria contact formation. Transmission electron microscopic observation confirms VES mediated ER-mitochondria contact while fluorescence microscopic analysis revealed that VES increased mitochondria-associated ER membrane (MAM) formation. Pre-treatment with the inositol 1,4,5-triphosphate receptor (IP3R) antagonist 2-aminoethyl diphenylborinate (2-APB) decreased VES-induced MAM formation, suggesting the involvement of VES-induced Ca2+ efflux from ER in MAM formation. The ER IP3R receptor is known to interact with voltage-dependent anion channels (VDAC) via the chaperone glucose-regulated protein 75 kDa (GRP75) to bring ER and mitochondria nearby. Although we revealed that VES treatment does not affect GRP75 protein level, it increases GRP75 localization in the MAM. In addition, the inhibition of Ca2+ release from ER by 2-APB decreases GRP75 localization in the MAM, suggesting the possibility of Ca2+-induced conformational change of GRP75 that promotes formation of the IP3R-GRP75-VDAC complex and thereby encourages MAM formation. This study identifies the mechanism of VES-induced enhanced Ca2+ transfer from ER to mitochondria, which causes mitochondrial Ca2+ overload leading to apoptosis. |
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| AbstractList | Vitamin E succinate (VES) is an esterified form of natural α-tocopherol, has turned out to be novel anticancer agent. However, its anticancer mechanisms have not been illustrated. Previously, we reported VES mediated Ca²⁺ release from the endoplasmic reticulum (ER) causes mitochondrial Ca²⁺ overload, leading to mitochondrial depolarization and apoptosis. Here, we elucidated the mechanism of VES-induced Ca²⁺ transfer from ER to mitochondria by investigating the role of VES in ER-mitochondria contact formation. Transmission electron microscopic observation confirms VES mediated ER-mitochondria contact while fluorescence microscopic analysis revealed that VES increased mitochondria-associated ER membrane (MAM) formation. Pre-treatment with the inositol 1,4,5-triphosphate receptor (IP₃R) antagonist 2-aminoethyl diphenylborinate (2-APB) decreased VES-induced MAM formation, suggesting the involvement of VES-induced Ca²⁺ efflux from ER in MAM formation. The ER IP₃R receptor is known to interact with voltage-dependent anion channels (VDAC) via the chaperone glucose-regulated protein 75 kDa (GRP75) to bring ER and mitochondria nearby. Although we revealed that VES treatment does not affect GRP75 protein level, it increases GRP75 localization in the MAM. In addition, the inhibition of Ca²⁺ release from ER by 2-APB decreases GRP75 localization in the MAM, suggesting the possibility of Ca²⁺-induced conformational change of GRP75 that promotes formation of the IP₃R-GRP75-VDAC complex and thereby encourages MAM formation. This study identifies the mechanism of VES-induced enhanced Ca²⁺ transfer from ER to mitochondria, which causes mitochondrial Ca²⁺ overload leading to apoptosis. Vitamin E succinate (VES) is an esterified form of natural α-tocopherol, has turned out to be novel anticancer agent. However, its anticancer mechanisms have not been illustrated. Previously, we reported VES mediated Ca2+ release from the endoplasmic reticulum (ER) causes mitochondrial Ca2+ overload, leading to mitochondrial depolarization and apoptosis. Here, we elucidated the mechanism of VES-induced Ca2+ transfer from ER to mitochondria by investigating the role of VES in ER-mitochondria contact formation. Transmission electron microscopic observation confirms VES mediated ER-mitochondria contact while fluorescence microscopic analysis revealed that VES increased mitochondria-associated ER membrane (MAM) formation. Pre-treatment with the inositol 1,4,5-triphosphate receptor (IP3R) antagonist 2-aminoethyl diphenylborinate (2-APB) decreased VES-induced MAM formation, suggesting the involvement of VES-induced Ca2+ efflux from ER in MAM formation. The ER IP3R receptor is known to interact with voltage-dependent anion channels (VDAC) via the chaperone glucose-regulated protein 75 kDa (GRP75) to bring ER and mitochondria nearby. Although we revealed that VES treatment does not affect GRP75 protein level, it increases GRP75 localization in the MAM. In addition, the inhibition of Ca2+ release from ER by 2-APB decreases GRP75 localization in the MAM, suggesting the possibility of Ca2+-induced conformational change of GRP75 that promotes formation of the IP3R-GRP75-VDAC complex and thereby encourages MAM formation. This study identifies the mechanism of VES-induced enhanced Ca2+ transfer from ER to mitochondria, which causes mitochondrial Ca2+ overload leading to apoptosis.Vitamin E succinate (VES) is an esterified form of natural α-tocopherol, has turned out to be novel anticancer agent. However, its anticancer mechanisms have not been illustrated. Previously, we reported VES mediated Ca2+ release from the endoplasmic reticulum (ER) causes mitochondrial Ca2+ overload, leading to mitochondrial depolarization and apoptosis. Here, we elucidated the mechanism of VES-induced Ca2+ transfer from ER to mitochondria by investigating the role of VES in ER-mitochondria contact formation. Transmission electron microscopic observation confirms VES mediated ER-mitochondria contact while fluorescence microscopic analysis revealed that VES increased mitochondria-associated ER membrane (MAM) formation. Pre-treatment with the inositol 1,4,5-triphosphate receptor (IP3R) antagonist 2-aminoethyl diphenylborinate (2-APB) decreased VES-induced MAM formation, suggesting the involvement of VES-induced Ca2+ efflux from ER in MAM formation. The ER IP3R receptor is known to interact with voltage-dependent anion channels (VDAC) via the chaperone glucose-regulated protein 75 kDa (GRP75) to bring ER and mitochondria nearby. Although we revealed that VES treatment does not affect GRP75 protein level, it increases GRP75 localization in the MAM. In addition, the inhibition of Ca2+ release from ER by 2-APB decreases GRP75 localization in the MAM, suggesting the possibility of Ca2+-induced conformational change of GRP75 that promotes formation of the IP3R-GRP75-VDAC complex and thereby encourages MAM formation. This study identifies the mechanism of VES-induced enhanced Ca2+ transfer from ER to mitochondria, which causes mitochondrial Ca2+ overload leading to apoptosis. |
| ArticleNumber | 130485 |
| Author | Ray, Manobendro Nath Kogure, Kentaro Kiyofuji, Michiko Ozono, Mizune |
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| Cites_doi | 10.1017/S0954422407202938 10.1242/jcs.095455 10.1016/j.jbc.2021.101368 10.1016/j.semcancer.2015.04.002 10.1017/S0007114512001882 10.1038/s41571-020-0341-y 10.1006/bbrc.2000.3237 10.1016/j.canlet.2010.04.002 10.3390/cancers11081087 10.1016/bs.apcsb.2021.02.007 10.3390/biom8020042 10.1016/S0304-4165(01)00168-4 10.1016/S0969-2126(97)00197-4 10.1016/j.ijpharm.2021.120457 10.1016/j.bpj.2010.10.016 10.1038/s41419-018-0416-1 10.1016/j.biopha.2005.06.005 10.1074/jbc.M110.210393 10.1186/s12885-015-1394-7 10.1038/nature11910 10.1083/jcb.200608073 10.1038/s41419-017-0179-0 10.1016/j.molcel.2010.06.029 10.3390/antiox11050989 10.3177/jnsv.65.S104 10.1111/febs.16623 10.1038/onc.2008.69 10.7150/ijbs.71571 10.1023/A:1016017832146 10.1074/jbc.275.20.15305 10.1038/s41419-017-0237-7 10.1038/leu.2011.216 10.1038/nrm3412 10.15252/embj.2021108272 |
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| References | Rieusset (10.1016/j.bbagen.2023.130485_bb0015) 2018; 9 Kogure (10.1016/j.bbagen.2023.130485_bb0145) 2019; 65 Martinvalet (10.1016/j.bbagen.2023.130485_bb0030) 2018; 9 Csordás (10.1016/j.bbagen.2023.130485_bb0135) 2010; 39 Li (10.1016/j.bbagen.2023.130485_bb0055) 2022; 18 Yan (10.1016/j.bbagen.2023.130485_bb0115) 2015; 15 Modesti (10.1016/j.bbagen.2023.130485_bb0060) 2021 M.P.K. and S.H (10.1016/j.bbagen.2023.130485_bb0070) 2018; 176 Lim (10.1016/j.bbagen.2023.130485_bb0005) 2019; 11 Ran (10.1016/j.bbagen.2023.130485_bb0045) 2000; 275 Sotomayor-Pérez (10.1016/j.bbagen.2023.130485_bb0180) 2011; 286 Tiwary (10.1016/j.bbagen.2023.130485_bb0170) 2021; 297 Ray (10.1016/j.bbagen.2023.130485_bb0130) 2022; 290 Kogure (10.1016/j.bbagen.2023.130485_bb0095) 2001; 1528 Brigelius-Flohé (10.1016/j.bbagen.2023.130485_bb0160) 2006; 19 Tiwary (10.1016/j.bbagen.2023.130485_bb0050) 2021; 297 Chenal (10.1016/j.bbagen.2023.130485_bb0185) 2010; 99 Marchi (10.1016/j.bbagen.2023.130485_bb0025) 1837; 2014 Zhang (10.1016/j.bbagen.2023.130485_bb0065) 2023; 9 Dong (10.1016/j.bbagen.2023.130485_bb0100) 2008; 27 Szalai (10.1016/j.bbagen.2023.130485_bb0195) 2000; 275 Dos Santos (10.1016/j.bbagen.2023.130485_bb0105) 2012; 26 Huang (10.1016/j.bbagen.2023.130485_bb0125) 2013; 109 Tameire (10.1016/j.bbagen.2023.130485_bb0090) 2015; 33 Tucker (10.1016/j.bbagen.2023.130485_bb0150) 2005; 59 Sriram (10.1016/j.bbagen.2023.130485_bb0190) 1997; 5 Galli (10.1016/j.bbagen.2023.130485_bb0155) 2022; 11 Çoku (10.1016/j.bbagen.2023.130485_bb0075) 2022; 41 Kluckova (10.1016/j.bbagen.2023.130485_bb0110) 1827; 2013 Huang (10.1016/j.bbagen.2023.130485_bb0120) 2010; 296 Liang (10.1016/j.bbagen.2023.130485_bb0085) 2021; 600 Bravo (10.1016/j.bbagen.2023.130485_bb0165) 2011; 124 Grzybowska (10.1016/j.bbagen.2023.130485_bb0175) 2018; 8 Hamasaki (10.1016/j.bbagen.2023.130485_bb0020) 2013; 495 Giamogante (10.1016/j.bbagen.2023.130485_bb0035) 2021; 126 Szabadkai (10.1016/j.bbagen.2023.130485_bb0040) 2006; 175 Carneiro (10.1016/j.bbagen.2023.130485_bb0010) 2020; 17 Rizzuto (10.1016/j.bbagen.2023.130485_bb0200) 2012; 13 Kerkhofs (10.1016/j.bbagen.2023.130485_bb0080) 2018; 9 Bonina (10.1016/j.bbagen.2023.130485_bb0140) 1996; 13 |
| References_xml | – volume: 19 start-page: 174 year: 2006 ident: 10.1016/j.bbagen.2023.130485_bb0160 article-title: Bioactivity of vitamin E publication-title: Nutr. Res. Rev. doi: 10.1017/S0954422407202938 – volume: 124 start-page: 2511 year: 2011 ident: 10.1016/j.bbagen.2023.130485_bb0165 article-title: Increased ER-mitochondrial coupling promotes mitochondrial respiration and bioenergetics during early phases of ER stress publication-title: J. Cell Sci. doi: 10.1242/jcs.095455 – volume: 297 year: 2021 ident: 10.1016/j.bbagen.2023.130485_bb0050 article-title: GRP75 mediates endoplasmic reticulum–mitochondria coupling during palmitate-induced pancreatic β-cell apoptosis publication-title: J. Biol. Chem. doi: 10.1016/j.jbc.2021.101368 – start-page: 1 year: 2021 ident: 10.1016/j.bbagen.2023.130485_bb0060 article-title: Mitochondrial ca 2 + signaling in health publication-title: Dis. Ther. – volume: 33 start-page: 3 year: 2015 ident: 10.1016/j.bbagen.2023.130485_bb0090 article-title: Cell intrinsic and extrinsic activators of the unfolded protein response in cancer: mechanisms and targets for therapy publication-title: Semin. Cancer Biol. doi: 10.1016/j.semcancer.2015.04.002 – volume: 109 start-page: 727 year: 2013 ident: 10.1016/j.bbagen.2023.130485_bb0125 article-title: Crosstalk between endoplasmic reticulum stress and oxidative stress in apoptosis induced by α-tocopheryl succinate in human gastric carcinoma cells publication-title: Br. J. Nutr. doi: 10.1017/S0007114512001882 – volume: 17 start-page: 395 year: 2020 ident: 10.1016/j.bbagen.2023.130485_bb0010 article-title: Targeting apoptosis in cancer therapy publication-title: Nat. Rev. Clin. Oncol. doi: 10.1038/s41571-020-0341-y – volume: 275 start-page: 174 year: 2000 ident: 10.1016/j.bbagen.2023.130485_bb0045 article-title: Extramitochondrial localization of Mortalin/mthsp70/PBP74/GRP75 publication-title: Biochem. Biophys. Res. Commun. doi: 10.1006/bbrc.2000.3237 – volume: 296 start-page: 123 year: 2010 ident: 10.1016/j.bbagen.2023.130485_bb0120 article-title: Endoplasmic reticulum stress contributes to vitamin E succinate-induced apoptosis in human gastric cancer SGC-7901 cells publication-title: Cancer Lett. doi: 10.1016/j.canlet.2010.04.002 – volume: 11 start-page: 1 year: 2019 ident: 10.1016/j.bbagen.2023.130485_bb0005 article-title: Novel apoptosis-inducing agents for the treatment of cancer, a new arsenal in the toolbox publication-title: Cancers (Basel) doi: 10.3390/cancers11081087 – volume: 126 start-page: 307 year: 2021 ident: 10.1016/j.bbagen.2023.130485_bb0035 article-title: Apoptotic signals at the endoplasmic reticulum-mitochondria interface publication-title: Adv. Protein Chem. Struct. Biol. doi: 10.1016/bs.apcsb.2021.02.007 – volume: 8 year: 2018 ident: 10.1016/j.bbagen.2023.130485_bb0175 article-title: Calcium-binding proteins with disordered structure and their role in secretion, storage, and cellular signaling publication-title: Biomolecules. doi: 10.3390/biom8020042 – volume: 1528 start-page: 25 year: 2001 ident: 10.1016/j.bbagen.2023.130485_bb0095 article-title: Superoxide is responsible for apoptosis in rat vascular smooth muscle cells induced by α-tocopheryl hemisuccinate publication-title: Biochim. Biophys. Acta, Gen. Subj. doi: 10.1016/S0304-4165(01)00168-4 – volume: 9 start-page: 1 year: 2023 ident: 10.1016/j.bbagen.2023.130485_bb0065 article-title: Synergistic mechanism between the endoplasmic reticulum and mitochondria and their crosstalk with other organelles publication-title: Cell Death Dis. – volume: 176 start-page: 100 year: 2018 ident: 10.1016/j.bbagen.2023.130485_bb0070 article-title: Balancing ER-mitochondrial Ca2+ fluxes in health and disease publication-title: Physiol. Behav. – volume: 297 year: 2021 ident: 10.1016/j.bbagen.2023.130485_bb0170 article-title: GRP75 mediates endoplasmic reticulum-mitochondria coupling during palmitate-induced pancreatic β-cell apoptosis publication-title: J. Biol. Chem. doi: 10.1016/j.jbc.2021.101368 – volume: 5 start-page: 403 year: 1997 ident: 10.1016/j.bbagen.2023.130485_bb0190 article-title: Human Hsp70 molecular chaperone binds two calcium ions within the ATPase domain publication-title: Structure. doi: 10.1016/S0969-2126(97)00197-4 – volume: 600 year: 2021 ident: 10.1016/j.bbagen.2023.130485_bb0085 article-title: Vitamin E succinate with multiple functions: a versatile agent in nanomedicine-based cancer therapy and its delivery strategies publication-title: Int. J. Pharm. doi: 10.1016/j.ijpharm.2021.120457 – volume: 99 start-page: 3744 year: 2010 ident: 10.1016/j.bbagen.2023.130485_bb0185 article-title: Calcium-induced folding and stabilization of the intrinsically disordered RTX domain of the CyaA roxin publication-title: Biophys. J. doi: 10.1016/j.bpj.2010.10.016 – volume: 9 start-page: 1 year: 2018 ident: 10.1016/j.bbagen.2023.130485_bb0015 article-title: The role of endoplasmic reticulum-mitochondria contact sites in the control of glucose homeostasis: an update publication-title: Cell Death Dis. doi: 10.1038/s41419-018-0416-1 – volume: 59 start-page: 380 year: 2005 ident: 10.1016/j.bbagen.2023.130485_bb0150 article-title: Alpha-tocopherol: roles in prevention and therapy of human disease publication-title: Biomed. Pharmacother. doi: 10.1016/j.biopha.2005.06.005 – volume: 286 start-page: 16997 year: 2011 ident: 10.1016/j.bbagen.2023.130485_bb0180 article-title: Calcium-induced folding of intrinsically disordered repeat-in-toxin (RTX) motifs via changes of protein charges and oligomerization states publication-title: J. Biol. Chem. doi: 10.1074/jbc.M110.210393 – volume: 15 start-page: 1 year: 2015 ident: 10.1016/j.bbagen.2023.130485_bb0115 article-title: Mitochondrially targeted vitamin E succinate efficiently kills breast tumour-initiating cells in a complex II-dependent manner publication-title: BMC Cancer doi: 10.1186/s12885-015-1394-7 – volume: 495 start-page: 389 year: 2013 ident: 10.1016/j.bbagen.2023.130485_bb0020 article-title: Autophagosomes form at ER-mitochondria contact sites publication-title: Nature. doi: 10.1038/nature11910 – volume: 175 start-page: 901 year: 2006 ident: 10.1016/j.bbagen.2023.130485_bb0040 article-title: Chaperone-mediated coupling of endoplasmic reticulum and mitochondrial Ca2+ channels publication-title: J. Cell Biol. doi: 10.1083/jcb.200608073 – volume: 9 year: 2018 ident: 10.1016/j.bbagen.2023.130485_bb0080 article-title: Emerging molecular mechanisms in chemotherapy: Ca2+ signaling at the mitochondria-associated endoplasmic reticulum membranes publication-title: Cell Death Dis. doi: 10.1038/s41419-017-0179-0 – volume: 39 start-page: 121 year: 2010 ident: 10.1016/j.bbagen.2023.130485_bb0135 article-title: Imaging Interorganelle contacts and local calcium dynamics at the ER-mitochondrial Interface publication-title: Mol. Cell doi: 10.1016/j.molcel.2010.06.029 – volume: 11 start-page: 1 year: 2022 ident: 10.1016/j.bbagen.2023.130485_bb0155 article-title: Vitamin E (alpha-tocopherol) metabolism and nutrition in chronic kidney disease publication-title: Antioxidants. doi: 10.3390/antiox11050989 – volume: 65 start-page: S104 year: 2019 ident: 10.1016/j.bbagen.2023.130485_bb0145 article-title: Biological functions of α-tocopheryl succinate publication-title: J. Nutr. Sci. Vitaminol. (Tokyo) doi: 10.3177/jnsv.65.S104 – volume: 290 start-page: 1027 year: 2022 ident: 10.1016/j.bbagen.2023.130485_bb0130 article-title: Only one carbon difference determines the pro-apoptotic activity of α -tocopheryl esters publication-title: FEBS J. doi: 10.1111/febs.16623 – volume: 2014 start-page: 461 year: 1837 ident: 10.1016/j.bbagen.2023.130485_bb0025 article-title: The endoplasmic reticulum–mitochondria connection: one touch, multiple functions publication-title: Biochim. Biophys. Acta Bioenerg. – volume: 27 start-page: 4324 year: 2008 ident: 10.1016/j.bbagen.2023.130485_bb0100 article-title: α-Tocopheryl succinate induces apoptosis by targeting ubiquinone-binding sites in mitochondrial respiratory complex II publication-title: Oncogene. doi: 10.1038/onc.2008.69 – volume: 18 start-page: 2914 year: 2022 ident: 10.1016/j.bbagen.2023.130485_bb0055 article-title: GRP75-faciliated mitochondria-associated ER membrane (MAM) integrity controls cisplatin-resistance in ovarian cancer patients publication-title: Int. J. Biol. Sci. doi: 10.7150/ijbs.71571 – volume: 13 start-page: 1343 year: 1996 ident: 10.1016/j.bbagen.2023.130485_bb0140 article-title: Transport of alpha-tocopherol and its derivatives through erythrocyte membranes publication-title: Pharm. Res. doi: 10.1023/A:1016017832146 – volume: 275 start-page: 15305 year: 2000 ident: 10.1016/j.bbagen.2023.130485_bb0195 article-title: Calcium signal transmission between ryanodine receptors and mitochondria publication-title: J. Biol. Chem. doi: 10.1074/jbc.275.20.15305 – volume: 9 year: 2018 ident: 10.1016/j.bbagen.2023.130485_bb0030 article-title: The role of the mitochondria and the endoplasmic reticulum contact sites in the development of the immune responses publication-title: Cell Death Dis. doi: 10.1038/s41419-017-0237-7 – volume: 26 start-page: 451 year: 2012 ident: 10.1016/j.bbagen.2023.130485_bb0105 article-title: (+)α-Tocopheryl succinate inhibits the mitochondrial respiratory chain complex I and is as effective as arsenic trioxide or ATRA against acute promyelocytic leukemia in vivo publication-title: Leukemia. doi: 10.1038/leu.2011.216 – volume: 2013 start-page: 552 year: 1827 ident: 10.1016/j.bbagen.2023.130485_bb0110 article-title: Mitochondrial complex II, a novel target for anti-cancer agents publication-title: Biochim. Biophys. Acta Bioenerg. – volume: 13 start-page: 566 year: 2012 ident: 10.1016/j.bbagen.2023.130485_bb0200 article-title: Mitochondria as sensors and regulators of calcium signalling publication-title: Nat. Rev. Mol. Cell Biol. doi: 10.1038/nrm3412 – volume: 41 start-page: 1 year: 2022 ident: 10.1016/j.bbagen.2023.130485_bb0075 article-title: Reduced ER–mitochondria connectivity promotes neuroblastoma multidrug resistance publication-title: EMBO J. doi: 10.15252/embj.2021108272 |
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| Snippet | Vitamin E succinate (VES) is an esterified form of natural α-tocopherol, has turned out to be novel anticancer agent. However, its anticancer mechanisms have... |
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| SubjectTerms | alpha-tocopherol antagonists antineoplastic agents apoptosis calcium endoplasmic reticulum esterification fluorescence microscopy inositols mitochondria protein content succinic acid transmission electron microscopy |
| Title | Vitamin E succinate mediated apoptosis by juxtaposing endoplasmic reticulum and mitochondria |
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