Tags

Type your tag names separated by a space and hit enter

Involvement of activator protein-1 (AP-1) in induction of apoptosis by vitamin E succinate in human breast cancer cells.
Mol Carcinog. 1997 Jul; 19(3):180-90.MC

Abstract

The purpose of this study was to document induction of apoptosis by vitamin E succinate (VES; RRR-alpha-tocopheryl succinate) in human breast cancer cells in culture and to characterize potential c-jun involvement. VES at 18.8 microM (10 micrograms/mL) induced DNA synthesis arrest, reduced total cell numbers, and induced apoptosis in estrogen receptor-positive and estrogen-responsive MCF-7 human breast cancer cells. VES at 10 micrograms/mL induced apoptosis in greater than 60% of cells within 3 d of treatment. Apoptosis was documented by detection of fragmented or condensed nuclei in 4',6-diamindino-2-phenylindole-stained cells, detection of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeled DNA, and DNA laddering. Analyses of mRNA and protein levels of candidate molecules involved in apoptosis showed that MCF-7 cells treated with VES exhibited elevated and persistent expression of c-jun. MCF-7 cells stably transfected with a dominant-negative interfering mutant c-jun, TAM-67, and expressing high levels of mutant jun exhibited approximately 50% blockage of VES-mediated apoptosis. In addition to increased c-jun expression after VES treatment, VES-treated MCF-7 cells exhibited elevated activator protein-1 (AP-1) binding activity. Comparisons of AP-1 binding factors by super-shift analyses with jun-specific antibodies in cells sensitive to VES-induced apoptosis (empty-vector control 7-1 cells) and cells resistant to VES-induced apoptosis (TAM-67-containing TAM-9 cells) showed that the sensitive cells expressed c-jun and jun D and the resistant cells TAM-67 AP-1 binding proteins after VES treatment. These studies suggested that c-jun may be involved in the apoptotic process initiated by VES treatment of human MCF-7 breast cancer cells.

Authors+Show Affiliations

Genetics Institute, 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 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

9254885

Citation

Zhao, B, et al. "Involvement of Activator Protein-1 (AP-1) in Induction of Apoptosis By Vitamin E Succinate in Human Breast Cancer Cells." Molecular Carcinogenesis, vol. 19, no. 3, 1997, pp. 180-90.
Zhao B, Yu W, Qian M, et al. Involvement of activator protein-1 (AP-1) in induction of apoptosis by vitamin E succinate in human breast cancer cells. Mol Carcinog. 1997;19(3):180-90.
Zhao, B., Yu, W., Qian, M., Simmons-Menchaca, M., Brown, P., Birrer, M. J., Sanders, B. G., & Kline, K. (1997). Involvement of activator protein-1 (AP-1) in induction of apoptosis by vitamin E succinate in human breast cancer cells. Molecular Carcinogenesis, 19(3), 180-90.
Zhao B, et al. Involvement of Activator Protein-1 (AP-1) in Induction of Apoptosis By Vitamin E Succinate in Human Breast Cancer Cells. Mol Carcinog. 1997;19(3):180-90. PubMed PMID: 9254885.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of activator protein-1 (AP-1) in induction of apoptosis by vitamin E succinate in human breast cancer cells. AU - Zhao,B, AU - Yu,W, AU - Qian,M, AU - Simmons-Menchaca,M, AU - Brown,P, AU - Birrer,M J, AU - Sanders,B G, AU - Kline,K, PY - 1997/7/1/pubmed PY - 2000/6/20/medline PY - 1997/7/1/entrez SP - 180 EP - 90 JF - Molecular carcinogenesis JO - Mol. Carcinog. VL - 19 IS - 3 N2 - The purpose of this study was to document induction of apoptosis by vitamin E succinate (VES; RRR-alpha-tocopheryl succinate) in human breast cancer cells in culture and to characterize potential c-jun involvement. VES at 18.8 microM (10 micrograms/mL) induced DNA synthesis arrest, reduced total cell numbers, and induced apoptosis in estrogen receptor-positive and estrogen-responsive MCF-7 human breast cancer cells. VES at 10 micrograms/mL induced apoptosis in greater than 60% of cells within 3 d of treatment. Apoptosis was documented by detection of fragmented or condensed nuclei in 4',6-diamindino-2-phenylindole-stained cells, detection of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeled DNA, and DNA laddering. Analyses of mRNA and protein levels of candidate molecules involved in apoptosis showed that MCF-7 cells treated with VES exhibited elevated and persistent expression of c-jun. MCF-7 cells stably transfected with a dominant-negative interfering mutant c-jun, TAM-67, and expressing high levels of mutant jun exhibited approximately 50% blockage of VES-mediated apoptosis. In addition to increased c-jun expression after VES treatment, VES-treated MCF-7 cells exhibited elevated activator protein-1 (AP-1) binding activity. Comparisons of AP-1 binding factors by super-shift analyses with jun-specific antibodies in cells sensitive to VES-induced apoptosis (empty-vector control 7-1 cells) and cells resistant to VES-induced apoptosis (TAM-67-containing TAM-9 cells) showed that the sensitive cells expressed c-jun and jun D and the resistant cells TAM-67 AP-1 binding proteins after VES treatment. These studies suggested that c-jun may be involved in the apoptotic process initiated by VES treatment of human MCF-7 breast cancer cells. SN - 0899-1987 UR - https://www.unboundmedicine.com/medline/citation/9254885/Involvement_of_activator_protein_1__AP_1__in_induction_of_apoptosis_by_vitamin_E_succinate_in_human_breast_cancer_cells_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0899-1987&date=1997&volume=19&issue=3&spage=180 DB - PRIME DP - Unbound Medicine ER -