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RRR-alpha-tocopheryl succinate inhibits EL4 thymic lymphoma cell growth by inducing apoptosis and DNA synthesis arrest.
Nutr Cancer. 1997; 27(1):92-101.NC

Abstract

RRR-alpha-tocopheryl succinate (vitamin E succinate, VES) treatment of murine EL4 T lymphoma cells induced the cells to undergo apoptosis. After 48 hours of VES treatment at 20 micrograms/ml, 95% of cells were apoptotic. Evidence for the induction of apoptosis by VES treatments is based on staining of DNA for detection of chromatin condensation/fragmentation, two-color flow-cytometric analyses of DNA content, and end-labeled DNA and electrophoretic analyses for detection of DNA ladder formation. VES-treated EL4 cells were blocked in the G1 cell cycle phase; however, apoptotic cells came from all cell cycle phases. Analyses of mRNA expression of genes involved in apoptosis revealed decreased c-myc and increased bcl-2, c-fos, and c-jun mRNAs within three to six hours after treatment. Western analyses showed increased c-Jun, c-Fos, and Bcl-2 protein levels. Electrophoretic mobility shift assays showed increased AP-1 binding at 6, 12, and 24 hours after treatment and decreased c-Myc binding after 12 and 24 hours of VES treatment. Treatments of EL4 cells with VES+RRR-alpha-to-copherol reduced apoptosis without effecting DNA synthesis arrest. Treatments of EL4 cells with VES+rac-6-hydroxyl-2, 5,7,8-tetramethyl-chroman-2-carboxylic acid, butylated hydroxytoluene, or butylated hydroxyanisole had no effect on apoptosis or DNA synthesis arrest caused by VES treatments. Analyses of bcl-2, c-myc, c-jun, and c-fos mRNA levels in cells receiving VES + RRR-alpha-tocopherol treatments showed no change from cells receiving VES treatments alone, implying that these changes are correlated with VES treatments but are not causal for apoptosis. However, treatments with VES + RRR-alpha-tocopherol decreased AP-1 binding to consensus DNA oligomer, suggesting AP-1 involvement in apoptosis induced by VES treatments.

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Publisher Full Text

Authors+Show Affiliations

Yu W
Genetics Institute, University of Texas at Austin 78712-1097, USA.
Sanders BG
No affiliation info available
Kline K
No affiliation info available

MeSH

AnimalsApoptosisBase SequenceBlotting, NorthernBlotting, WesternCell CycleDNA, NeoplasmFlow CytometryGene Expression Regulation, NeoplasticLymphomaMiceMice, Inbred C57BLProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junProto-Oncogene Proteins c-mycRNA, MessengerThymidineThymus NeoplasmsTocopherolsTranscription Factor AP-1Tumor Cells, CulturedVitamin E

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8970189

Citation

Yu, W, et al. "RRR-alpha-tocopheryl Succinate Inhibits EL4 Thymic Lymphoma Cell Growth By Inducing Apoptosis and DNA Synthesis Arrest." Nutrition and Cancer, vol. 27, no. 1, 1997, pp. 92-101.
Yu W, Sanders BG, Kline K. RRR-alpha-tocopheryl succinate inhibits EL4 thymic lymphoma cell growth by inducing apoptosis and DNA synthesis arrest. Nutr Cancer. 1997;27(1):92-101.
Yu, W., Sanders, B. G., & Kline, K. (1997). RRR-alpha-tocopheryl succinate inhibits EL4 thymic lymphoma cell growth by inducing apoptosis and DNA synthesis arrest. Nutrition and Cancer, 27(1), 92-101.
Yu W, Sanders BG, Kline K. RRR-alpha-tocopheryl Succinate Inhibits EL4 Thymic Lymphoma Cell Growth By Inducing Apoptosis and DNA Synthesis Arrest. Nutr Cancer. 1997;27(1):92-101. PubMed PMID: 8970189.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - RRR-alpha-tocopheryl succinate inhibits EL4 thymic lymphoma cell growth by inducing apoptosis and DNA synthesis arrest. AU - Yu,W, AU - Sanders,B G, AU - Kline,K, PY - 1997/1/1/pubmed PY - 1997/1/1/medline PY - 1997/1/1/entrez SP - 92 EP - 101 JF - Nutrition and cancer JO - Nutr Cancer VL - 27 IS - 1 N2 - RRR-alpha-tocopheryl succinate (vitamin E succinate, VES) treatment of murine EL4 T lymphoma cells induced the cells to undergo apoptosis. After 48 hours of VES treatment at 20 micrograms/ml, 95% of cells were apoptotic. Evidence for the induction of apoptosis by VES treatments is based on staining of DNA for detection of chromatin condensation/fragmentation, two-color flow-cytometric analyses of DNA content, and end-labeled DNA and electrophoretic analyses for detection of DNA ladder formation. VES-treated EL4 cells were blocked in the G1 cell cycle phase; however, apoptotic cells came from all cell cycle phases. Analyses of mRNA expression of genes involved in apoptosis revealed decreased c-myc and increased bcl-2, c-fos, and c-jun mRNAs within three to six hours after treatment. Western analyses showed increased c-Jun, c-Fos, and Bcl-2 protein levels. Electrophoretic mobility shift assays showed increased AP-1 binding at 6, 12, and 24 hours after treatment and decreased c-Myc binding after 12 and 24 hours of VES treatment. Treatments of EL4 cells with VES+RRR-alpha-to-copherol reduced apoptosis without effecting DNA synthesis arrest. Treatments of EL4 cells with VES+rac-6-hydroxyl-2, 5,7,8-tetramethyl-chroman-2-carboxylic acid, butylated hydroxytoluene, or butylated hydroxyanisole had no effect on apoptosis or DNA synthesis arrest caused by VES treatments. Analyses of bcl-2, c-myc, c-jun, and c-fos mRNA levels in cells receiving VES + RRR-alpha-tocopherol treatments showed no change from cells receiving VES treatments alone, implying that these changes are correlated with VES treatments but are not causal for apoptosis. However, treatments with VES + RRR-alpha-tocopherol decreased AP-1 binding to consensus DNA oligomer, suggesting AP-1 involvement in apoptosis induced by VES treatments. SN - 0163-5581 UR - https://www.unboundmedicine.com/medline/citation/8970189/RRR_alpha_tocopheryl_succinate_inhibits_EL4_thymic_lymphoma_cell_growth_by_inducing_apoptosis_and_DNA_synthesis_arrest_ L2 - https://www.tandfonline.com/doi/full/10.1080/01635589709514508 DB - PRIME DP - Unbound Medicine ER -