In:
Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 1040-1040
Abstract:
Lung cancer is leading cause of all cancer deaths. Although omega-3 polyunsaturated fatty acids (ω3-PUFAs) have been reported to inhibit cell growth in several cancers, the anti-cancer mechanism of ω3-PUFAs on lung cancer is still unclear. In this study, we have investigated the mechanism of anti-cancer action of DHA, one of ω3-PUFAs, in A549 human non-small cell lung cancer (NSCLC) cell line. Following treatment of DHA, the viability of A549 cells was decreased in a dose-dependent manner. DHA induced apoptotic cell death as revealed by increased cleaved PARP, TUNEL positive cells and subG1 population. The amounts of PI3K and phospho-Akt proteins were decreased after DHA treatment dose-dependent manner. In addition, DHA decreased the level of phospho-phosphatase and tensin homolog deleted on chromosome ten (p-PTEN) protein, which is an inactive form of PTEN. Moreover, transient transfection of constitutive active Akt cDNA and full length of Akt cDNA into A549 cells partially restored DHA-dependent inhibition of cell growth compared with the cells transfected with kinase dead form of Akt. Taken together, these data suggest that inhibition of PI3K/Akt signaling pathway may be related to anti-cancer action of DHA in A549 human NSCLC cells. Therefore, utilization of DHA may represent a potential effective therapy for the chemoprevention and treatment of human non-small cell lung cancer. [This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (R13-2007-020-01000-0)] Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meetin g of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1040. doi:10.1158/1538-7445.AM2011-1040
Type of Medium:
Online Resource
ISSN:
0008-5472
,
1538-7445
DOI:
10.1158/1538-7445.AM2011-1040
Language:
English
Publisher:
American Association for Cancer Research (AACR)
Publication Date:
2011
detail.hit.zdb_id:
2036785-5
detail.hit.zdb_id:
1432-1
detail.hit.zdb_id:
410466-3
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