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Role of extracellular signal-regulated kinase pathway in RRR-alpha-tocopheryl succinate-induced differentiation of human MDA-MB-435 breast cancer cells.

Role of extracellular signal-regulated kinase pathway in RRR-alpha-tocopheryl succinate-induced differentiation of human MDA-MB-435 breast cancer cells. Research Abstract Details 

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  • Role of extracellular signal-regulated kinase pathway in RRR-alpha-tocopheryl succinate-induced differentiation of human MDA-MB-435 breast cancer cells. Abstract Text:

    huihong youHuihong You,weiping yuWeiping Yu,debbie munoz-medellinDebbie Munoz-Medellin,powel h brownPowel H Brown,bob g sandersBob G Sanders,kimberly klineKimberly Kline,

    RRR-alpha-tocopheryl succinate (vitamin E succinate, VES) induces differentiation of human breast cancer cells. Previous studies ruled out transforming growth factor-beta and c-jun N-terminal kinase involvement in VES-induced differentiation but implicated extracellular signal-regulated kinases (ERKs). Here we show that dominant-negative mutants of either mitogen-activated protein kinase kinase (MEK) 1 or ERK1 blocked VES-induced differentiation of MDA-MB-435 cells, as measured by induction of cytokeratin 18 and p21 (Waf1/Cip1) proteins. Blockage of c-jun protein expression using c-jun antisense oligonucleotides or expression of an inducible dominant-negative c-jun mutant protein inhibited VES-induced differentiation. Elevated expression of wild-type c-jun alone was sufficient to induce cellular differentiation. A role for p21 (Waf1/Cip1) is implicated, in that p21 antisense oligomers blocked VES-induced differentiation. In summary, MEK1, ERK1, the transcription factor c-jun, and the cyclin-dependent kinase inhibitor p21 (Waf1/Cip1) play a part in VES-induced differentiation of human MDA-MB-435 breast cancer cells.

    Role of extracellular signal-regulated kinase pathway in RRR-alpha-tocopheryl succinate-induced differentiation of human MDA-MB-435 breast cancer cells. Publishing Authors By Initials

    h youH You,w yuW Yu,d munoz-medellinD Munoz-Medellin,ph brownPH Brown,bg sandersBG Sanders,k klineK Kline,

    For similar heterocyclic compounds: heterocyclic compounds, 2-ring: benzopyrans: vitamin e research abstracts see: heterocyclic compounds: heterocyclic compounds, 2-ring: benzopyrans: vitamin e research

    PUBMED ID PMID:

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    Role of extracellular signal-regulated kinase pathway in RRR-alpha-tocopheryl succinate-induced differentiation of human MDA-MB-435 breast cancer cells. Journal Published:

    PUBLICATION TYPE: Research Support, U.S. Gov't,

    Journal: Molecular carcinogenesis

    VOLUME: 33

    Page Numbers: 228-36

    Journal Abbreviation: Mol. Carcinog.

    ISSN: 0899-1987

    DAY: 19

    MONTH: Apr

    YEAR: 2002

    Role of extracellular signal-regulated kinase pathway in RRR-alpha-tocopheryl succinate-induced differentiation of human MDA-MB-435 breast cancer cells. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8811105

    Role of extracellular signal-regulated kinase pathway in RRR-alpha-tocopheryl succinate-induced differentiation of human MDA-MB-435 breast cancer cells. Keywords Mesh Terms:

    KEYWORDS: Vitamin E

    MESH TERMS: pharmacology

    Chemical & Substance for Abstract: Role of extracellular signal-regulated kinase pathway in RRR-alpha-tocopheryl succinate-induced differentiation of human MDA-MB-435 breast cancer cells. Information

    Substance Name: Protein-Serine-Threonine Kinases

    Registry Number: EC 2.7.11.1

    Grant and Affiliation Information for Role of extracellular signal-regulated kinase pathway in RRR-alpha-tocopheryl succinate-induced differentiation of human MDA-MB-435 breast cancer cells.

    AFFILIATION: Department of Molecular Genetics and Microbiology/C0900 School of Biological Sciences, The University of Texas at Austin, 78712-1097, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCI

    GRANT: CA59739

    ACRONYM: CA

    MEDLINETA: Mol Carcinog

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    DATABASENAME:

    ACCESSION NUMBER:

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