Repository of Research and Investigative Information

Repository of Research and Investigative Information

Zahedan University of Medical Sciences

Docosahexaenoic acid sensitizes Ramos cells to Gamma-irradiation-induced apoptosis through involvement of PPAR-gamma activation and NF-kappa B suppression

(2008) Docosahexaenoic acid sensitizes Ramos cells to Gamma-irradiation-induced apoptosis through involvement of PPAR-gamma activation and NF-kappa B suppression. Molecular and Cellular Biochemistry. pp. 113-120. ISSN 0300-8177

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Official URL: <Go to ISI>://WOS:000259440500013

Abstract

Gamma-irradiation (Gamma-IR) resistance is a character of many malignant cells that decreases the efficacy of radiotherapy. Although ionizing radiation activates multiple cellular factors that vary depending on dose and tissue specificity, the activation of nuclear factor-kappa B appears to be a well-conserved response in tumor cells exposed to Gamma-IR which can lead to the inhibition of radiation-induced apoptosis. Thus, inhibition of NF-kappa B activation is an important strategy to abolish radioresistance. Recently, we have demonstrated that docosahexaenoic acid (DHA; 22:6 n-3 polyunsaturated fatty acids)-induced apoptosis may occur via ligand-dependent transcription factor, peroxisome proliferator-activated receptors-gamma. Moreover, many reports described that activation of PPAR-gamma can lead to the induction of apoptosis through NF-kappa B inhibition. Therefore, we addressed the mechanism that NF-kappa B is a downstream target of DHA and may be involved in the process of radiosensitization. Ramos cells are a highly radiation-resistant and p53-deficient Burkitt's lymphoma cell line. The results of present study showed that cotreatment of Ramos cells with low doses of DHA and Gamma-IR leads to marked phosphorylation of I kappa B and translocation of p65/NF-kappa B to nucleus in parallel with increase in apoptosis. Preincubation of the cells with GW9662, a selective antagonist for PPAR-gamma, significantly prevented NF-kappa B activation profile. Taken together, these results suggest that low concentration of DHA inhibited Gamma-IR-induced activation of NF-kappa B and sensitized Ramos cells to IR-induced cytotoxicity. Pretreatment of Ramos cells with GW9662 abrogated the ability of DHA to inhibit Gamma-IR-induced activation of NF-kappa B and diminished the DHA radiosensitizing effect indicating that PPAR-gamma may act as a mediator of DHA in inhibition of NF-kappa B. Taken together, these results suggest that low concentration of DHA inhibited Gamma-IR-induced activation of NF-kappa B and sensitized Ramos cells to IR-induced cytotoxicity. Pretreatment of Ramos cells with GW9662 abrogated the ability of DHA to inhibit Gamma-IR-induced activation of NF-kappa B and diminished the DHA radiosensitizing effect indicating that PPAR-gamma may act as a mediator of DHA in inhibition of NF-kappa B.

Item Type: Article
Keywords: DHA ionizing irradiation PPAR-gamma NF-kappa B p53 receptor-gamma ionizing-radiation cancer inhibition proteins kinase gene agonists alpha lines Cell Biology
Page Range: pp. 113-120
Journal or Publication Title: Molecular and Cellular Biochemistry
Journal Index: ISI
Volume: 317
Number: 1-2
Identification Number: https://doi.org/10.1007/s11010-008-9838-x
ISSN: 0300-8177
Depositing User: خانم مهدیه رضائی پور
URI: http://eprints.zaums.ac.ir/id/eprint/2839

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