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学科主题: 临床医学
题名:
Antineoplastic effects of 15(S)-hydroxyeicosatetraenoic acid and 13-S-hydroxyoctadecadienoic acid in non-small cell lung cancer
作者: Li, Ming-Yue1; Yuan, Hui-Ling1,2; Ko, Fanny W. S.3; Wu, Bin4; Long, Xiang5; Du, Jing5; Wu, Jun4; Ng, Calvin S. H.1; Wan, Innes Y. P.1; Mok, Tony S. K.6; Hui, David S. C.3; Underwood, Malcolm J.1; Chen, George G.1
关键词: 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE) ; 13-S-hydroxyoctadecadienoic acid (13(S)-HODE) ; 15-lipoxygenase 1 (15-LOX-1) ; 15-lipoxygenase 2 (15-LOX-2) ; lung cancer ; peroxisome proliferator-activated receptor (PPAR)
刊名: CANCER
发表日期: 2015-09-01
DOI: 10.1002/cncr.29547
卷: suppl.17, 期:SI, 页:3130-3145
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Oncology
研究领域[WOS]: Oncology
关键词[WOS]: ACTIVATED RECEPTOR-GAMMA ; PPAR-GAMMA ; EXPRESSION ; GROWTH ; 15-LIPOXYGENASE-2 ; APOPTOSIS ; THIAZOLIDINEDIONES ; PROGRESSION ; INHIBITION ; RADIATION
英文摘要:

BACKGROUNDPrevious 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.

METHODSNSCLC 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.

RESULTSThe application of exogenous 13(S)-HODE and 15(S)-HETE significantly enhanced the activity of peroxisome proliferator-activated receptor (PPAR), 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.

CONCLUSIONSThis study has demonstrated that exogenous or endogenous 13(S)-HODE and 15(S)-HETE can functionally inhibit NSCLC, likely by activating PPAR. 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 PPAR ligands. Cancer 2015;121:3130-45. (c) 2015 American Cancer Society.

语种: 英语
所属项目编号: 462613
项目资助者: Research Grants Council of the Hong Kong Special Administrative Region (Chinese University of Hong Kong)
WOS记录号: WOS:000360761900013
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内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/55824
Appears in Collections:北京大学深圳医院_期刊论文

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作者单位: 1.Dongguan Peoples Hosp, Dept Breast Surg, Dongguan, Peoples R China
2.Peking Univ, Shenzhen Hosp, Shenzhen, Peoples R China
3.Chinese Univ Hong Kong, Prince Wales Hosp, Dept Surg, Hong Kong, Hong Kong, Peoples R China
4.Chinese Univ Hong Kong, Prince Wales Hosp, Dept Med & Therapeut, Hong Kong, Hong Kong, Peoples R China
5.Guang Dong Med Coll, Affiliated Hosp, Dept Resp Med, Zhanjiang, Peoples R China
6.Chinese Univ Hong Kong, Prince Wales Hosp, Dept Clin Oncol, Hong Kong, Hong Kong, Peoples R China

Recommended Citation:
Li, Ming-Yue,Yuan, Hui-Ling,Ko, Fanny W. S.,et al. Antineoplastic effects of 15(S)-hydroxyeicosatetraenoic acid and 13-S-hydroxyoctadecadienoic acid in non-small cell lung cancer[J]. CANCER,2015,suppl.17(SI):3130-3145.
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