Abstract
Eicosapentaenoic acid (EPA) is an unsaturated fatty acid with various bioactivities, including antitumor effects. We previously reported a synergistic antitumor effect of cisplatin (CDDP) and EPA. Here, we examined the underlying mechanism. The human oesophageal cancer cell line TE-1 was treated with the combination of EPA and CDDP. Nuclear translocation of NF-κB, a transcription factor involved in cytokine production, was detected by immunohistochemistry. IL-6 levels were measured by ELISA. Apoptosis and cell cycle distribution were evaluated by flow cytometry. Nuclear translocation of NF-κB in TE-1 cells was synergistically decreased by CDDP and EPA. IL-6 production was increased following treatment with CDDP, but treatment with EPA decreased IL-6 levels. Apoptosis was synergistically induced by CDDP and EPA. A G2/M cell cycle arrest was observed with the combination of CDDP and 150 μM EPA, and S phase arrest with the combination of CDDP and 100 μM EPA. The combination of CDDP and EPA synergistically suppresses NF-κB nuclear translocation and increases apoptosis by inducing cell cycle arrest at the S or G2/M phase.
Highlights
In our previous study, we reported several effects of Eicosapentaenoic acid (EPA) on the TE-1 human oesophageal cancer cell line [13]
To clarify the mechanism of the synergistic antitumor effect of the combined use of EPA and CDDP, we examined the role of NF-ĸB and investigated cytokine production, apoptosis and cell cycle arrest in response to the combination treatment
The rate of NF-ĸB nuclear stained cells in TE-1 cells treated with 0, 2 and 5 μg/ml of CDDP was 8.2%, 9.5% and 8.4%, respectively, and there were no significant differences between these rates
Summary
We reported several effects of EPA on the TE-1 human oesophageal cancer cell line [13]. Lipopolysaccharide promotes the nuclear translocation of the NF-ĸB transcription factor [14]. Lipopolysaccharide induces cytokine production in TE-1 cells, and this activity was inhibited by EPA [13]. We further found that EPA promoted apoptosis and controlled tumor proliferation through inhibition of NF-ĸB nuclear translocation and activation. Several studies examined the combined use of EPA and anticancer agents and found that EPA showed a synergistic antitumor effect when combined with docetaxel, paclitaxel or cisplatin (CDDP) [15]. To clarify the mechanism of the synergistic antitumor effect of the combined use of EPA and CDDP, we examined the role of NF-ĸB and investigated cytokine production, apoptosis and cell cycle arrest in response to the combination treatment
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