Antineoplastic effects of 15(S)-hydroxyeicosatetraenoic acid and 13-S-hydroxyoctadecadienoic acid in non-small cell lung cancer

Cancer
Ming-Yue LiGeorge G Chen

Abstract

Previous studies have shown that the levels of 15-lipoxygenase 1 (15-LOX-1) and 15-LOX-2 as well as their metabolites 13-S-hydroxyoctadecadienoic acid (13(S)-HODE) and 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE) are significantly reduced in smokers with non-small cell lung carcinoma (NSCLC). Furthermore, animal model experiments have indicated that the reduction of these molecules occurs before the establishment of cigarette smoking carcinogen-induced lung tumors, and this suggests roles in lung tumorigenesis. However, the functions of these molecules remain unknown in NSCLC. NSCLC cells were treated with exogenous 13(S)-HODE and 15(S)-HETE, and then the ways in which they affected cell function were examined. 15-LOX-1 and 15-LOX-2 were also overexpressed in tumor cells to restore these 2 enzymes to generate endogenous 13(S)-HODE and 15(S)-HETE before cell function was assessed. 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 caspases 9 and 3. The overexpression of 15-LOX-1 and 15-LOX-2 obviously promoted the endogenous levels of 13(S)-HODE and 15(S)-HETE, which w...Continue Reading

References

Jan 9, 2003·The Journal of Immunology : Official Journal of the American Association of Immunologists·Pattabhiraman Shankaranarayanan, Santosh Nigam
Oct 21, 2003·International Journal of Cancer. Journal International Du Cancer·George G ChenThomas C Spelsberg
Apr 1, 2005·Neoplasia : an International Journal for Oncology Research·Vemparala SubbarayanDavid G Menter
Mar 7, 2006·Critical Reviews in Clinical Laboratory Sciences·Ming-Yue LiGeorge G Chen
Apr 7, 2009·American Journal of Respiratory Cell and Molecular Biology·Ming-Yue LiGeorge G Chen
Sep 17, 2010·Journal of Cell Science·Shawn B Bratton, Guy S Salvesen
Oct 26, 2010·The Journal of Clinical Investigation·Rachel Wilson GoeheCharles E Chalfant
Mar 1, 2011·Lung Cancer : Journal of the International Association for the Study of Lung Cancer·Ajaya Kumar RekaVenkateshwar G Keshamouni
May 3, 2011·American Journal of Physiology. Lung Cellular and Molecular Physiology·Teodora NicolaYiu-Fai Chen
Dec 29, 2011·Frontiers in Bioscience (Landmark Edition)·Gregory T Robbins, Daotai Nie
Apr 3, 2012·Current Cancer Drug Targets·M-Y LiG G Chen
Dec 12, 2012·Molecular Cancer Therapeutics·Robert RamerBurkhard Hinz
Dec 12, 2013·British Journal of Clinical Pharmacology·Richard M TurnerYoon K Loke
Mar 7, 2014·Expert Opinion on Investigational Drugs·Hardik JoshiC S Ramaa
Mar 8, 2014·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Juan LiYe Yang
Apr 16, 2014·Cell Cycle·Mahipal V SuraneniDean G Tang
May 29, 2014·Cell Cycle·Yande Guo, Daotai Nie
Jul 19, 2014·American Journal of Physiology. Gastrointestinal and Liver Physiology·Marisol CabralJuan José Moreno
Sep 24, 2014·Cancer Prevention Research·Jing PanMing You

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Citations

Aug 20, 2019·Journal of Experimental & Clinical Cancer Research : CR·Ming-Yue LiGeorge G Chen
Feb 13, 2020·Journal of Translational Medicine·Li-Zhong LiuMing-Yue Li
Jan 13, 2021·Translational Psychiatry·Roel J T MockingRobert K Naviaux

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