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I.Y. Wan
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P1.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 233)
- Event: WCLC 2015
- Type: Poster
- Track: Biology, Pathology, and Molecular Testing
- Presentations: 1
- Moderators:
- Coordinates: 9/07/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P1.04-082 - Anti-Neoplastic Effects of 15(S)-HETE and 13(S)-HODE in Lung Cancer (ID 299)
09:30 - 09:30 | Author(s): I.Y. Wan
- Abstract
Background:
Previous studies have shown that the levels of 15-lipoxygenase-1(15-LOX-1),15-lipoxygenase-2(15-LOX-2) and their metabolites 13(S)-HODE and 15(S)-HETE are significantly reduced in human non-small cell lung carcinoma (NSCLC). Furthermore, animal model experiments indicate that the reduction of these molecules occurs before the establishment of lung tumor, suggesting their roles in lung tumorigenesis. However, the functions of these molecules remain unknown in NSCLC.
Methods:
We treated NSCLC cells with exogenous 13(S)-HODE and 15(S)-HETE and then examined how they affected cell functions. We also over-expressed 15-LOX-1 and 15-LOX-2 in tumor cells to restore these two enzymes to generate endogenous 13(S)-HODE and 15(S)-HETE before the cell function was assessed.
Results:
The application of exogenous 13(S)-HODE and 15(S)-HETE significantly enhanced the activity of peroxisome proliferator-activated receptor-γ(PPARγ), inhibited cell proliferation, induced apoptosis, and activated caspase-9 and caspase-3. The overexpression of 15-LOX-1 and 15-LOX-2 could obviously promote the endogenous levels of 13(S)-HODE and 15(S)-HETE, which were demonstrated to be more effective in the inhibition of NSCLC.
Conclusion:
We have demonstrated that exogenous or endogenous 13(S)-HODE and 15(S)-HETE can functionally inhibit NSCLC likely by activating PPARγ. The restoration of 15-LOXs activities to increase the production of endogenous 15(S)-HETE and 13(S)-HODE may offer a novel research direction for the molecular targeting treatment of NSCLC and avoid potential side-effects associated with the application of synthetic PPARγ ligands.
