دورية أكاديمية
Antineoplastic effects of 15(S)-hydroxyeicosatetraenoic acid and 13-S-hydroxyoctadecadienoic acid in non-small cell lung cancer.
| العنوان: | Antineoplastic effects of 15(S)-hydroxyeicosatetraenoic acid and 13-S-hydroxyoctadecadienoic acid in non-small cell lung cancer. |
|---|---|
| المؤلفون: | Li MY; Department of Surgery, Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong, People's Republic of China., Yuan HL; Department of Surgery, Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong, People's Republic of China.; Department of Breast Surgery, Dongguan People's Hospital, Dongguan, People's Republic of China., Ko FW; Department of Medicine and Therapeutics, Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong, People's Republic of China., Wu B; Department of Respiratory Medicine, Affiliated Hospital of Guang Dong Medical College, Zhanjiang, People's Republic of China., Long X; Shenzhen Hospital, Peking University, Shenzhen, People's Republic of China., Du J; Shenzhen Hospital, Peking University, Shenzhen, People's Republic of China., Wu J; Department of Respiratory Medicine, Affiliated Hospital of Guang Dong Medical College, Zhanjiang, People's Republic of China., Ng CS; Department of Surgery, Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong, People's Republic of China., Wan IY; Department of Surgery, Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong, People's Republic of China., Mok TS; Department of Clinical Oncology, Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong, People's Republic of China., Hui DS; Department of Medicine and Therapeutics, Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong, People's Republic of China., Underwood MJ; Department of Surgery, Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong, People's Republic of China., Chen GG; Department of Surgery, Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong, People's Republic of China. |
| المصدر: | Cancer [Cancer] 2015 Sep 01; Vol. 121 Suppl 17, pp. 3130-45. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Wiley Country of Publication: United States NLM ID: 0374236 Publication Model: Print Cited Medium: Internet ISSN: 1097-0142 (Electronic) Linking ISSN: 0008543X NLM ISO Abbreviation: Cancer Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: <2005- >: Hoboken, NJ : Wiley Original Publication: New York [etc.] Published for the American Cancer Society by J. Wiley [etc.] |
| مواضيع طبية MeSH: | Arachidonate 15-Lipoxygenase/*biosynthesis , Carcinoma, Non-Small-Cell Lung/*drug therapy , Fatty Acids, Unsaturated/*administration & dosage , Hydroxyeicosatetraenoic Acids/*administration & dosage, Antineoplastic Agents/administration & dosage ; Apoptosis/drug effects ; Arachidonate 15-Lipoxygenase/genetics ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; PPAR gamma/genetics |
| مستخلص: | Background: 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. Methods: 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. 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 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 were demonstrated to be more effective in the inhibition of NSCLC. Conclusions: This study has demonstrated that exogenous or endogenous 13(S)-HODE and 15(S)-HETE can functionally inhibit NSCLC, likely by activating PPARγ. The restoration of 15-LOX activity to increase the production of endogenous 15(S)-HETE and 13(S)-HODE may offer a novel research direction for molecular targeting treatment of smoking-related NSCLC. This strategy can potentially avoid side effects associated with the application of synthetic PPARγ ligands. (© 2015 American Cancer Society.) |
| فهرسة مساهمة: | Keywords: 13-S-hydroxyoctadecadienoic acid (13(S)-HODE); 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE); 15-lipoxygenase 1 (15-LOX-1); 15-lipoxygenase 2 (15-LOX-2); lung cancer; peroxisome proliferator-activated receptor γ (PPARγ) |
| المشرفين على المادة: | 0 (Antineoplastic Agents) 0 (Fatty Acids, Unsaturated) 0 (Hydroxyeicosatetraenoic Acids) 0 (PPAR gamma) 0 (hydroxyoctadecadienoic acid) EC 1.13.11.33 (ALOX15B protein, human) EC 1.13.11.33 (Arachidonate 15-Lipoxygenase) |
| تواريخ الأحداث: | Date Created: 20150903 Date Completed: 20151125 Latest Revision: 20150903 |
| رمز التحديث: | 20240829 |
| DOI: | 10.1002/cncr.29547 |
| PMID: | 26331820 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1097-0142 |
|---|---|
| DOI: | 10.1002/cncr.29547 |