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RRR-alpha-tocopheryl succinate induction of prolonged activation of c-jun amino-terminal kinase and c-jun during induction of apoptosis in human MDA-MB-435 breast cancer cells.
Mol Carcinog 1998; 22(4):247-57MC

Abstract

We have demonstrated that RRR-alpha-tocopheryl succinate (10 microg/mL vitamin E succinate (VES) treatment of estrogen receptor-negative MDA-MB-435 human breast cancer cells induces 9, 19, 51, and 72% apoptotic cells on days 1-4, respectively, after treatment, which involves transforming growth factor-beta signaling. Here, we show that VES-triggered apoptosis of MDA-MB-435 cells induced prolonged elevated expression of c-jun mRNA and protein (neither of which was caused by major increases in stability) and also induced enhanced activator protein-1 (AP-1) binding to the consensus DNA oligomer. Furthermore, VES treatments resulted in increased AP-1 transactivation activity, as measured with an AP-1 promoter/luciferase reporter construct and by the measurement of increased mRNA expression of the AP-1-dependent endogenous gene collagenase. Evidence of VES-induced involvement of the c-jun amino-terminal kinase in these AP-1-dependent events was suggested by data showing prolonged activity of this kinase, as measured by a kinase assay using glutathione S-transferase-c-jun as the substrate. The c-jun-dependent transcriptional activity was verified by cotransfection of a chimeric transcription factor having a galactose 4 DNA-binding domain coupled with the transactivation domain of c-jun plus the reporter plasmid 5X GAL4-luciferase. MDA-MB-435 cells infected with an adenovirus expression vector containing the TAM-67 sequence for dominant/negative-acting mutant c-jun or transiently transfected with c-jun antisense exhibited a 50-77% reduction in VES-mediated apoptosis as compared with control adenovirus-infected or control sense oligomer-transfected cells.

Authors+Show Affiliations

Department of Zoology, The University of Texas at Austin, 78712-1097, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

9726817

Citation

Yu, W, et al. "RRR-alpha-tocopheryl Succinate Induction of Prolonged Activation of C-jun Amino-terminal Kinase and C-jun During Induction of Apoptosis in Human MDA-MB-435 Breast Cancer Cells." Molecular Carcinogenesis, vol. 22, no. 4, 1998, pp. 247-57.
Yu W, Simmons-Menchaca M, You H, et al. RRR-alpha-tocopheryl succinate induction of prolonged activation of c-jun amino-terminal kinase and c-jun during induction of apoptosis in human MDA-MB-435 breast cancer cells. Mol Carcinog. 1998;22(4):247-57.
Yu, W., Simmons-Menchaca, M., You, H., Brown, P., Birrer, M. J., Sanders, B. G., & Kline, K. (1998). RRR-alpha-tocopheryl succinate induction of prolonged activation of c-jun amino-terminal kinase and c-jun during induction of apoptosis in human MDA-MB-435 breast cancer cells. Molecular Carcinogenesis, 22(4), pp. 247-57.
Yu W, et al. RRR-alpha-tocopheryl Succinate Induction of Prolonged Activation of C-jun Amino-terminal Kinase and C-jun During Induction of Apoptosis in Human MDA-MB-435 Breast Cancer Cells. Mol Carcinog. 1998;22(4):247-57. PubMed PMID: 9726817.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - RRR-alpha-tocopheryl succinate induction of prolonged activation of c-jun amino-terminal kinase and c-jun during induction of apoptosis in human MDA-MB-435 breast cancer cells. AU - Yu,W, AU - Simmons-Menchaca,M, AU - You,H, AU - Brown,P, AU - Birrer,M J, AU - Sanders,B G, AU - Kline,K, PY - 1998/9/3/pubmed PY - 2000/6/20/medline PY - 1998/9/3/entrez SP - 247 EP - 57 JF - Molecular carcinogenesis JO - Mol. Carcinog. VL - 22 IS - 4 N2 - We have demonstrated that RRR-alpha-tocopheryl succinate (10 microg/mL vitamin E succinate (VES) treatment of estrogen receptor-negative MDA-MB-435 human breast cancer cells induces 9, 19, 51, and 72% apoptotic cells on days 1-4, respectively, after treatment, which involves transforming growth factor-beta signaling. Here, we show that VES-triggered apoptosis of MDA-MB-435 cells induced prolonged elevated expression of c-jun mRNA and protein (neither of which was caused by major increases in stability) and also induced enhanced activator protein-1 (AP-1) binding to the consensus DNA oligomer. Furthermore, VES treatments resulted in increased AP-1 transactivation activity, as measured with an AP-1 promoter/luciferase reporter construct and by the measurement of increased mRNA expression of the AP-1-dependent endogenous gene collagenase. Evidence of VES-induced involvement of the c-jun amino-terminal kinase in these AP-1-dependent events was suggested by data showing prolonged activity of this kinase, as measured by a kinase assay using glutathione S-transferase-c-jun as the substrate. The c-jun-dependent transcriptional activity was verified by cotransfection of a chimeric transcription factor having a galactose 4 DNA-binding domain coupled with the transactivation domain of c-jun plus the reporter plasmid 5X GAL4-luciferase. MDA-MB-435 cells infected with an adenovirus expression vector containing the TAM-67 sequence for dominant/negative-acting mutant c-jun or transiently transfected with c-jun antisense exhibited a 50-77% reduction in VES-mediated apoptosis as compared with control adenovirus-infected or control sense oligomer-transfected cells. SN - 0899-1987 UR - https://www.unboundmedicine.com/medline/citation/9726817/RRR_alpha_tocopheryl_succinate_induction_of_prolonged_activation_of_c_jun_amino_terminal_kinase_and_c_jun_during_induction_of_apoptosis_in_human_MDA_MB_435_breast_cancer_cells_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0899-1987&date=1998&volume=22&issue=4&spage=247 DB - PRIME DP - Unbound Medicine ER -