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RRR-alpha-tocopheryl succinate enhances TGF-beta 1, -beta 2, and -beta 3 and TGF-beta R-II expression by human MDA-MB-435 breast cancer cells.
Nutr Cancer. 1996; 26(2):237-50.NC

Abstract

The proliferation of MDA-MB-435 human breast cancer cells was inhibited by RRR-alpha-tocopheryl succinate (vitamin E succinate, VES). Conditioned media (CM) from VES growth-inhibited cells contained potent antiproliferative activity, part of which is contributed by transforming growth factor-beta (TGF-beta) isoforms. Antibody neutralization analysis, employing TGF-beta isoform-specific antibody reagents, showed that TGF-beta 1, -beta 2, and -beta 3 were present in the CM from VES-treated cells. Culturing MDA-MB-435 cells with VES did not alter the levels of constitutively expressed 2.4-kb TGF-beta 1, 3.0- and 4.0-kb TGF-beta 2, or 1.2- and 3.5-kb TGF-beta 3 mRNA transcripts. Inhibition of DNA synthesis by MDA-MB-435 cells was increased by combinations of suboptimal levels of VES and purified TGF-beta 1. VES-treated MDA-MB-435 cells exhibited enhanced binding of radiolabeled TGF-beta 1, and Western immunoblotting analyses showed that VES treatment enhanced TGF-beta type II receptor protein expression. TGF-beta type I receptor protein levels were not modified by VES treatments. Although the mRNA transcript for the 5.5-kb TGF-beta type II receptor was upregulated after four hours of treatment with VES, this treatment did not modify the 6.5-kb TGF-beta type I or the 6.5-kb TGF-beta type II receptor mRNAs. Results demonstrate that biologically active TGF-beta 1, -beta 2, -beta 3 and levels of TGF-beta type II receptor expressed by human breast cancer cells are enhanced by VES treatment.

Authors+Show Affiliations

Division of Nutritional Sciences, 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, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

8875561

Citation

Charpentier, A, et al. "RRR-alpha-tocopheryl Succinate Enhances TGF-beta 1, -beta 2, and -beta 3 and TGF-beta R-II Expression By Human MDA-MB-435 Breast Cancer Cells." Nutrition and Cancer, vol. 26, no. 2, 1996, pp. 237-50.
Charpentier A, Simmons-Menchaca M, Yu W, et al. RRR-alpha-tocopheryl succinate enhances TGF-beta 1, -beta 2, and -beta 3 and TGF-beta R-II expression by human MDA-MB-435 breast cancer cells. Nutr Cancer. 1996;26(2):237-50.
Charpentier, A., Simmons-Menchaca, M., Yu, W., Zhao, B., Qian, M., Heim, K., Sanders, B. G., & Kline, K. (1996). RRR-alpha-tocopheryl succinate enhances TGF-beta 1, -beta 2, and -beta 3 and TGF-beta R-II expression by human MDA-MB-435 breast cancer cells. Nutrition and Cancer, 26(2), 237-50.
Charpentier A, et al. RRR-alpha-tocopheryl Succinate Enhances TGF-beta 1, -beta 2, and -beta 3 and TGF-beta R-II Expression By Human MDA-MB-435 Breast Cancer Cells. Nutr Cancer. 1996;26(2):237-50. PubMed PMID: 8875561.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - RRR-alpha-tocopheryl succinate enhances TGF-beta 1, -beta 2, and -beta 3 and TGF-beta R-II expression by human MDA-MB-435 breast cancer cells. AU - Charpentier,A, AU - Simmons-Menchaca,M, AU - Yu,W, AU - Zhao,B, AU - Qian,M, AU - Heim,K, AU - Sanders,B G, AU - Kline,K, PY - 1996/1/1/pubmed PY - 1996/1/1/medline PY - 1996/1/1/entrez SP - 237 EP - 50 JF - Nutrition and cancer JO - Nutr Cancer VL - 26 IS - 2 N2 - The proliferation of MDA-MB-435 human breast cancer cells was inhibited by RRR-alpha-tocopheryl succinate (vitamin E succinate, VES). Conditioned media (CM) from VES growth-inhibited cells contained potent antiproliferative activity, part of which is contributed by transforming growth factor-beta (TGF-beta) isoforms. Antibody neutralization analysis, employing TGF-beta isoform-specific antibody reagents, showed that TGF-beta 1, -beta 2, and -beta 3 were present in the CM from VES-treated cells. Culturing MDA-MB-435 cells with VES did not alter the levels of constitutively expressed 2.4-kb TGF-beta 1, 3.0- and 4.0-kb TGF-beta 2, or 1.2- and 3.5-kb TGF-beta 3 mRNA transcripts. Inhibition of DNA synthesis by MDA-MB-435 cells was increased by combinations of suboptimal levels of VES and purified TGF-beta 1. VES-treated MDA-MB-435 cells exhibited enhanced binding of radiolabeled TGF-beta 1, and Western immunoblotting analyses showed that VES treatment enhanced TGF-beta type II receptor protein expression. TGF-beta type I receptor protein levels were not modified by VES treatments. Although the mRNA transcript for the 5.5-kb TGF-beta type II receptor was upregulated after four hours of treatment with VES, this treatment did not modify the 6.5-kb TGF-beta type I or the 6.5-kb TGF-beta type II receptor mRNAs. Results demonstrate that biologically active TGF-beta 1, -beta 2, -beta 3 and levels of TGF-beta type II receptor expressed by human breast cancer cells are enhanced by VES treatment. SN - 0163-5581 UR - https://www.unboundmedicine.com/medline/citation/8875561/RRR_alpha_tocopheryl_succinate_enhances_TGF_beta_1__beta_2_and__beta_3_and_TGF_beta_R_II_expression_by_human_MDA_MB_435_breast_cancer_cells_ L2 - https://www.tandfonline.com/doi/full/10.1080/01635589609514480 DB - PRIME DP - Unbound Medicine ER -