Gamma tocopherol upregulates the expression of 15-S-HETE and induces growth arrest through a PPAR gamma-dependent mechanism in PC-3 human prostate cancer cells.

Chronic inflammation and dietary fat consumption correlates with an increase in prostate cancer. Our previous studies in the colon have demonstrated that gamma -tocopherol treatment could upregulate the expression of peroxisome proliferator-activated preceptors (PPAR) gamma , a nuclear receptor invo...

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Publicado en:Nutrition & Cancer Vol. 61; no. 5; pp. 649 - 663
Autores principales: Campbell SE, Musich PR, Whaley SG, Stimmel JB, Leesnitzer LM, Dessus-Babus S, Duffourc M, Stone W, Newman RA, Yang P, Krishnan K
Formato: pictorial research tables/charts Journal Article
Publicado: Taylor & Francis Ltd Sep/Oct2009
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Sep/Oct2009
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      pub: Taylor & Francis Ltd
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        atl: Gamma tocopherol upregulates the expression of 15-S-HETE and induces growth arrest through a PPAR gamma-dependent mechanism in PC-3 human prostate cancer cells.
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        au:
          Campbell SE
          Musich PR
          Whaley SG
          Stimmel JB
          Leesnitzer LM
          Dessus-Babus S
          Duffourc M
          Stone W
          Newman RA
          Yang P
          Krishnan K
        affil: Department of Biochemistry, East Tennessee State University, P.O. Box 70851, Johnson City, TN 37614; campbese@etsu.edu
      sug:
        subj:
          Fatty Acids Therapeutic Use
          Prostatic Neoplasms Risk Factors
          Proteins
          Vitamin E Therapeutic Use
          Analysis of Variance
          Biological Assay Methods
          Blotting, Western
          Descriptive Statistics
          Enzyme-Linked Immunosorbent Assay
          Funding Source
          Neoplasms Physiopathology
          Nutrition
          Polymerase Chain Reaction
          Post Hoc Analysis
          Tissue Culture Techniques Methods
          Human
      ab: Chronic inflammation and dietary fat consumption correlates with an increase in prostate cancer. Our previous studies in the colon have demonstrated that gamma -tocopherol treatment could upregulate the expression of peroxisome proliferator-activated preceptors (PPAR) gamma , a nuclear receptor involved in fatty acid metabolism as well modulation of cell proliferation and differentiation. In this study, we explored the possibility that gamma -tocopherol could induce growth arrest in PC-3 prostate cancer cells through the regulation of fatty acid metabolism. Growth arrest (40%) and PPAR gamma mRNA and protein upregulation was achieved with gamma -tocopherol within 6 h. Gamma -Tocopherol-mediated growth arrest was demonstrated to be PPAR gamma dependent using the agonist GW9662 and a PPAR gamma dominant negative vector. Gamma -tocopherol was shown not to be a direct PPAR gamma ligand, but rather 15-S-HETE (an endogenous PPAR gamma ligand) was upregulated by gamma -tocopherol treatment. 15- Lipoxygenase-2, a tumor suppressor and the enzyme that converts arachidonic acid to 15-S-HETE, was upregulated at 3 h following gamma -tocopherol treatment. Expression of proteins downstream of the PPAR gamma pathway were examined. Cyclin D1, cyclin D3, bcl- 2, and NFkappa B proteins were found to be downregulated following gamma -tocopherol treatment. These data demonstrate that the growth arrest mediated by gamma -tocopherol follows a PPAR-gamma -dependent mechanism.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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