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  • American Association for Cancer Research (AACR)  (27)
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  • American Association for Cancer Research (AACR)  (27)
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  • 1
    Online Resource
    Online Resource
    Abstract 2071: Docosahexaenoic acid-induced apoptosis is directly linked to mitochondria-mediated reactive oxygen species production in human cervical cancer cells
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 2071-2071
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 2071-2071
    Abstract: Reactive oxygen species (ROS) produced by docosahexaenoic acid (DHA) have an important function in cancer cell death. However, the exact mechanism of ROS production, after DHA stimulation, is not clearly understood. Here, we determined that elevated levels of ROS generated by mitochondrial respiration is directly associated with DHA-induced cervical cancer cell death. The levels of caspase 3 activity, TUNEL-positive staining cells and Sub-G1 portion were markedly increased in DHA-treated cancer cells, suggesting that apoptosis is responsible for the DHA-induced cervical cancer cell death. Furthermore, DHA was able to induce both mitochondrial complex I substrate- and complex II substrate-supported mitochondrial ROS production in isolated mitochondria from rodent liver. Meanwhile, a reduction in oxygen consumption rate and an increase in mitochondrial ROS production as measured by MitoSOX, were also observed in DHA-treated cancer cells, indicating that DHA can directly act on mitochondrial respiration and enhance ROS generation. The role of DHA-induced mitochondrial ROS production in apoptosis was further identified by the findings that DHA reduced the mitochondrial membrane potential, resulting in cardiolipin oxidation and cytochrome c release from mitochondria, and that N-acetylcysteine, an antioxidant almost completely blocked these processes as well as ROS production occurred in mitochondria and remarkably reversed the apoptotic cell death triggered by DHA. From the results presented here, we conclude that mitochondria actively participate in the DHA-induced apoptotic cell death by the generation of mitochondrial ROS. (This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Ministry of Education, Science and Technology (2011-0006232 and 2011-0003060)). Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2071. doi:1538-7445.AM2012-2071
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-2071
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 2
    Online Resource
    Online Resource
    Abstract 1985: Omega-3 polyunsaturated fatty acids induce cell cytotoxicity through apoptosis and autophgy in brain cancer in vitro and in vivo
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1985-1985
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1985-1985
    Abstract: One of the most common and biologically aggressive of malignant astrocytic gliomas is glioblastoma (GBM). Studies have revealed a significant role of phosphatidylinositol-3-OH kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling activation during GBM development. Omega-3 polyunsaturated fatty acids (≥3-PUFAs) have been shown to inhibit several cancer cells growth such as breast cancer cells. Here, we examined the anticancer effect of α3-PUFAs in D54 malignant glioma (D54MG) cells. We show that docosahexaenoic acid (DHA), a α3-PUFA, induced apoptosis in D54MG cells, as confirmed by the formation of cleaved PARP, TUNEL assay and cytofluorometric analysis. DHA-treated D54MG cells also showed a significant increase in autophagic activity as revealed by LC3-II elevation, autophagic vesicles formation and autophagy flux assays, suggeting that both apoptosis and autophagy contribute to the DHA-induced tumor cell death. The DHA-induced cell death in D54MG cells was accompained by the activation of AMPK and decrease in the Akt phosphorylation. DHA also decreased the activity of mTOR and the level of its downstream molecule 4EBP as analyzed by the Western blot assay. DHA-induced apoptosis and autophagy were partially blocked by transient overexpression of Akt, supporting the inhibition of Akt being beneficial to the death of GBM cells. In in vivo studies, the growth of implanted murine GBM cells in Fat-1 transgenic mice, that can produce high levels of α3-PUFA, was significantly inhibited, and the apoptotic index was higher compared with wild type mice. Together, these results suggest that α3-FUFAs induce cell cytotoxicity through apoptosis and autophgy in brain 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(2011-0006232).] Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1985. doi:1538-7445.AM2012-1985
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-1985
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 3
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    Abstract 2255: DHA may enhance proteasome activity in human cervical cancer cells: Indirect modulation of proteasome by DHA
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 2255-2255
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 2255-2255
    Abstract: The omega-3 fatty acid, docosahexaenoic acid (DHA), has been shown to induce the proteasomal degradation of various cancer-associated molecules such as beta-catenin and estrogen receptor, implying its regulatory effect on proteasome. To verify this possible link between DHA and proteasome function, we explored the impacts of DHA on human papillomavirus-positive HeLa cervical cancer cells that constitutively express two known endogenous proteasome substrates E6 and E7 viral proteins. Exposure HeLa cells to DHA resulted in elevated proteasome activities along with decreased levels of E6/E7 viral proteins, and these effects of DHA were remarkably reversed in the presence of proteasome inhibitors, suggesting that DHA improves proteasome function in the cells and thereby accelerates the degradation of proteasome substrates. The DHA-induced increase in cellular proteasome activity was preceded by reactive oxygen species (ROS) overproduction and could be blocked by preincubation of the cells with ROS scavengers. Likewise, HeLa cells treated with exogenous ROS, H2O2, also exhibited significantly improved proteasome function. Unexpectedly, when the purified proteasome and whole-cell lysates isolated from HeLa cells were directly exposed to DHA or H2O2, such marked increases in proteasome activity were not seen. Taken together, these findings indicate that DHA may induce proteasome activation in cervical cancer cells mainly by indirect regulation of the proteasome. Citation Format: Kyu Lim, Kaipeng Jing, Soyeon Shin, Soyeon Jeong, Soyeon Kim, Gi-Ryang Kweon, Seung-Kiel Park, Tong Wu, Jong-Il Park. DHA may enhance proteasome activity in human cervical cancer cells: Indirect modulation of proteasome by DHA. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2255. doi:10.1158/1538-7445.AM2014-2255
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-2255
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
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  • 4
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    Abstract 4651: Docosahexaenoic acid-induced degradation of epidermal growth factor receptor through lysosome and ubiquitin/proteasomal system in human non-small cell lung cancer cells
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 4651-4651
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 4651-4651
    Abstract: Mutations in EGFR gene frequently occurr in lung cancer and their expressions are related to poor prognosis and drug resistance. Although docosahexaenoic acid (DHA) has anti-cancer activity, the underlying mechanism is not well known in human non-small cell lung cancer (NSCLC) yet. In this study, we show a molecular mechanism of DHA-induced degradation of EGFR in human NSCLC cells. To determine whether DHA modulates EGFR degradation, we used three NSCLC cell lines, which is A549 (EGFR WT), and two mutant cells (PC9 and H1975). We confirmed that the viability of three lung cancer cells was decreased by DHA in a dose- and time-dependent manner. DHA augmented EGFR degradation and its ubiquitin in all three cell lines. Indeed, DHA increased the levels of E3-ligase, c-cbl and endosome-related molecules (Rab5, EEA1, Rab7, and LAMP1). Chloroquin (CQ) effectively blocked the DHA-induced EGFR degradation. Moreover, knockdown of lysosome associated membrane protein (LAMP) by its siRNAs, which regulates lysosome fusion, partially prevented EGFR degradation induced by DHA, and co-localization of EGFR with lysosome in immunocytochemistry, suggesting that DHA-induced EGFR degradation is associated with lysosomal degradation. On the other hand, MG132 (proteasome inhibitor) also protected DHA-triggered EGFR degradation, demonstrating that proteasomes also contribute to EGFR degradation in response to DHA treatment. To confirm the effects of endogenous ω3-PUFAs on EGFR degradation, fat-1-stablyexpressing A549 (f-A549) and PC9 cells (f-PC9) were established (The cells express a C. elegansω3-desaturase converting ω6- to ω3-PUFAs endogenously). The level of EGFR was reduced in f-A549 and f-PC9 cells, indicating ω3-PUFAs diminish EGFR level. The cell growth was retarded and the tumorigenicity was inhibited in nude mice. In addition, EGFR levels were significantly decreased in tumor tissues from f-A549 and f-PC9 cells-bearing mice. Taken together, DHA may induce the degradation of EGFR through lysosome and ubiquitin/proteosomal system in EGFR WT and EGFR mutant NSCLC cells. Thus, these findings provide important preclinical evidence and molecular insight for utilization of ω3-PUFAs in the chemoprevention and treatment of human NSCLC.[This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (2007-0054932)] Citation Format: Soyeon Jeong, Kaipeng Jing, Soyeon Shin, Soyeon Kim, Young-Joo Jeon, Jun-Young Heo, Gi-Ryang Kweon, Seung-Kiel Park, Jong-Il Park, Kyu Lim. Docosahexaenoic acid-induced degradation of epidermal growth factor receptor through lysosome and ubiquitin/proteasomal system in human non-small cell lung cancer cells. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4651.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2016-4651
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
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  • 5
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    Abstract 1301: Anti-invasive and antimetastatic effects of ω3-polyunsaturated fatty acids through inhibition of NF-kB/matrix metalloproteinases in ovarian cancer cells
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 1301-1301
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 1301-1301
    Abstract: Ovarian cancer is leading cause of gene cological cancer death in the United States. It is reported that about 14,000 patients will die to ovarian cancer in United States, 2015. ω3- and ω6-PUFAs are considered as essential fatty acids because they cannot be synthesized in mammals. The ω3-desaturase (fat-1) converts ω6-PUFAs to ω3-PUFAs. Cancer cells and transgenic mice stably expressing fat-1 geneare useful models to study the anti-cancer effects of ω3-PUFAs. Here, we show anti-invasive and anti-metastatic action of ω3-PUFA in ovarian cancer.DHA significantly inhibited cell invasion and wound healing activity of human ovarian PA-1 cells. DHA also abolishedthe induction of matrix-metalloproteinases (MMPs) and cyclooxygenase (COX2) as well as the transactivity of NF-κB in PA-1 cells. When ID8 cells were subcutaneously implanted into fat-1 transgenic mice, the tumor size and volume were smallin comparison to wild-type mice. The growth inhibition of tumor was also confirmed with the increase in the level of TUNEL-positive cells. Additionally, when ID8 cells were injected via tail vein of fat1 mice, the lung metastasis was remarkably inhibited in fat-1 transgenic mice. Furthermore, the proliferation of fat-1-stably expressing PA-1 (f-PA-1) cells was more attenuated than that of cells expressing control vectors. The invasion and NF-κB/MMPs promoter activities were also decreased in f-PA-1 cells. These results suggest that ω3-PUFAs inhibit invasion and metastasis of ovarian cancer cells through inhibition of NF-κB/MMPs. Therefore, ω3-PUFAs may contribute an effective and safe therapeutic approach for the chemoprevention and treatment of human ovarian cancer. [This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (2007-0054932)] Citation Format: Soyeon Jeong, Kaipeng Jing, Soyeon Shin, Soyeon Kim, Young-Joo Jeon, Jun-Young Heo, Gi-Ryang Kweon, Seung-Kiel Park, Jong-Il Park, Kyu Lim. Anti-invasive and antimetastatic effects of ω3-polyunsaturated fatty acids through inhibition of NF-kB/matrix metalloproteinases in ovarian cancer cells. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1301.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2016-1301
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
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    detail.hit.zdb_id: 1432-1
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  • 6
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    Abstract 2110: Anti-invasive and antimetastatic actions of omega-3 polyunsaturated fatty acids in glioblastoma cells
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Research Vol. 77, No. 13_Supplement ( 2017-07-01), p. 2110-2110
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. 2110-2110
    Abstract: Glioblastoma (GBM) is the most aggressive and deadliest brain malignancy in adults. Despite of surgical techniques, radiotherapy and chemotherapy, GBM has remained an invariably lethal tumor with a median survival less than 15 months. Although the anticancer mechanisms of omega-3 polyunsaturated fatty acids (ω3-PUFAs) have been reported in several cancers, it is still unclear in brain cancer. Here, our data show the anti-invasive and anti-metastatic effects of ω3-PUFAs in GBM. Invasiveness using transwell chamber was inhibited by docosahexaenoic acid (DHA) treatment in D54MG and GL261 cells. In zymography, MMP-2 activity was suppressed by DHA in a dose dependent manner. MMP-2 promoter activity was also decreased. DHA inhibited both p-STAT3 and β-catenin levels that contribute to invasion by stimulating pro-invasion factors such as MMP-2. Additionally, fat-1 (ω3-desaturease) stable D54MG cell was established and the effect of the high level of ω3-PUFAs was investigated endogenously. The invasiveness were significantly inhibited in the fat-1 stable cells compared to control cell. Moreover, the metastasis in vivo was significantly reduced when GL261 mouse glioma cells were injected through tail vein into the fat-1 transgenic mice. In immunohistochemistry, intensity of p-STAT-3 and β-catenin were significantly weak in metastatic lung tumor from Fat-1 mice compared to wild type mice. These results indicate that anti-invasive and anti-metastatic actions of ω3-PUFA may be correlated with inhibition of MMP-2 through decrease of STAT3 and β-catenin in GBM cells. Thus, these findings provide important preclinical evidence and molecular insight for utilization of ω-3 PUFAs for the chemoprevention and treatment of human GBM. [This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (2007-0054932, NRF-2015R1D1A1A01056887) and by the framework of international cooperation program managed by National Research Foundation of Korea (2015K2A2A6002008)]. Citation Format: Soyeon Kim, Soyeon Shin, Soyeon Jeong, Seung-Hyeon Han, Yoon-Seon Yoo, Prashanta Silwal, Young-Joo Jeon, Jun-Young Heo, Gi-Ryang Kweon, Seung-Kiel Park, Jong-Il Park, Kyu Lim. Anti-invasive and antimetastatic actions of omega-3 polyunsaturated fatty acids in glioblastoma cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2110. doi:10.1158/1538-7445.AM2017-2110
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2017-2110
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
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  • 7
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    Abstract 1767: Anti-proliferative and anti-invasive action of omega-3 polyunsaturated fatty acids in stomach cancer cells
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 1767-1767
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 1767-1767
    Abstract: The American Cancer Society has been reported that about 22,220 cases of stomach cancer will be diagnosed and about 10,990 patients will die from this type of cancer in 2014. Omega-3 polyunsaturated fatty acids (ω3-PUFA), including docosahexaenoic acid (DHA) have been suggested to have anti-cancer effects by epidemiological and clinical studies. However, their underlying anti-cancer mechanisms are still unclear in stomach cancer. This study was designed to examine the impact of ω3-PUFA on stomach cancer and the molecular mechanism of their action. DHA reduced cells viability in a dose- and time-dependent manner in human stomach cancer cells including AGS cells. The DHA-induced cells death was in part due to apoptosis, since the cells exhibited increases of apoptotic markers including cleaved PARP and TUNEL-positive cells. DHA also led to autophagic vesicle formation an increase levels of lipidated form LC3B and stimulated the autophagic flux, indicating the involvement of both apoptosis and autophagy in the cytotoxic effect of stomach cancer cells by ω3-PUFA. Moreover, AGS stable cell expressing the ω3-desaturase (fat-1) gene (AGS-fsc) or control vector stable cell (AGS-csc) were eatablished, and the effect of endogenous high level of ω3-PUFA was investigated in AGS cells. The cell proliferation, invasion and colony-formation were inhibited in AGS-fsc compared to AGS-csc. Taken together, these results indicate that ω3-PUFA induce anti-cancer action is related to anti-proliferation and anti-invasive action in stomach cancer cells. Thus, utilization of ω3-PUFA may represent a promising therapeutic approach for chemoprevention and treatment of human stomach cancer. [This research was supported by Basic Science Research Program through the National Research Foundation of Korea(NRF) funded by the Ministry of Education(2014R1A1A2008915) and by the Korea government(MSIP) (No. 2007-0054932)] Citation Format: Soyeon Shin, Soyeon Jeong, Soyeon Kim, Jun-Young Heo, Gi-Ryang Kweon, Seung-Kiel Park, Jong-Il Park, Kyu Lim. Anti-proliferative and anti-invasive action of omega-3 polyunsaturated fatty acids in stomach cancer cells. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1767. doi:10.1158/1538-7445.AM2015-1767
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-1767
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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  • 8
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    Abstract 1901: Endogenous increase of omega-3 polyunsaturated fatty acids through expression of of ω3-desaturase gene inhibits tumorigenicity and metastasis of prostate cancer cells in vitro and in vivo
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 1901-1901
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 1901-1901
    Abstract: The ω3-desaturase (Fat-1) catalyzes the conversion ω6-polyunsaturated fatty acids (ω6-PUFAs) to ω3 polyunsaturated fatty acids (ω3-PUFAs) and increases the amount of ω3-PUFAs. It is known that ω3-PUFAs have anti-tumorigenic properties, while ω6-PUFAs accelerate tumorigenesis. Here, we report that endogenous increase of omega-3 polyunsaturated fatty acids through expression of fat-1 gene may inhibit tumorigenicity and metastasis of prostate cancer cells in vitro and in vivo. When mouse prostate cancer RM1 cells were implanted into mice, tumor size and volume were significantly reduced in Fat-1 transgenic mice (Fat-1 transgenic mice express a Caenorhabditis elegans ω3-desaturase converting ω6- to ω3-PUFAs endogenously.) compared with wild mice. In immunohistochemical analysis of tumors tissue of Fat-1 mice, apoptotic cells were markedly increased and angiogenesis significantly was reduced, compared with wild mice tumor. When RM1 cells were injected through tail vein, lung metastasis of RM1 cells was significantly inhibited in Fat-1 transgenic mice. On the other hand, the fat-1 stable RM1 cells (fRM1sc) were significantly inhibited the proliferation compared to the cells expressing the control vector (fRM1cc) and fRM1sc showed an increase in the proportion of cells in G2/M phase comparing with fRM1cc. Tumor growth of fRM1sc implanted into C57BL6 control mice was significantly decreased, and tumor tissues from fRM1sc implanted-animals showed an increase in the apoptotic index compared to fRM1cc. Moreover, the proliferation index and microvessel density were significantly decreased. Furthermore, transwell chamber assay for invasion indicated a reduction of cell invasion in the human prostate fPC3sc when compared with the fRM1cc. In Zymography, MMP-9 and MMP-2 activties were decrease in fPC3sc. These results suggest that expression of the fat-1 gene, thereby enhancing endogenous levels of ω3-PUFAs may prevent tumorigenicity and metastasis of prostate cancer cells. Additionally, transgenic mouse and a stable cell line of fat-1 gene are useful to study the anti-cancer effects of ω3-PUFAs. [This research was supported by the National Research Foundation of Korea(NRF) grant funded by the Korea government(MSIP) (No. 2007-0054932)] Citation Format: Soyeon Shin, Kaipeng Jing, Soyeon Jeong, Soyeon Kim, Yifan Dai, Tong Wu, Jun-Young Heo, Seung-Kiel Park, Gi-Ryang Kweon, Jong-Il Park, Kyu Lim. Endogenous increase of omega-3 polyunsaturated fatty acids through expression of of ω3-desaturase gene inhibits tumorigenicity and metastasis of prostate cancer cells in vitro and in vivo. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1901. doi:10.1158/1538-7445.AM2015-1901
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-1901
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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  • 9
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    Abstract 5121: Omega-3 polyunsaturated fatty acids induce apoptotic and autophagic cell death through inhibition of Akt/mTOR pathway in human oral cancer cells
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 5121-5121
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 5121-5121
    Abstract: Omega-3 polyunsaturated fatty acids (ω3-PUFAs) have been found to possess anticancer properties in a variety of cancer cell lines and animal models, but their effect in oral cancer remains unclear. This study was designed to examine the impact of ω3-PUFAs on oral cancer and the molecular mechanism of their action using in vitro and in vivo models. Exposure SCC4 and SCC9 human oral cancer cells to the ω3-PUFA docosahexaenoic acid (DHA) reduced cell viability in a dose- and time-dependent manner. The increase in cell death was due in part to apoptosis, since cells incubated with DHA exhibited elevated levels of apoptotic markers including cleaved PARP expression, subG1 DNA portion and TUNEL-positive nuclei. DHA treatment also led to autophagic vesicle formation and an increase in autophagic flux, indicating the involvement of both apoptosis and autophagy in the cytotoxic effect of ω3-PUFAs on oral cancer cells. Further experiments revealed that the concurrent activation of apoptosis and autophagy induced by DHA was linked to reactive oxygen species (ROS) overproduction and inhibition of Akt/mTOR signaling molecules. Moreover, stable SCC9 cell lines expressing the ω3-desaturase gene (SCC9-fsc) or control vector (SCC9-csc) were generated, and the effect of endogenous high level of ω3-PUFAs was investigated. The growth rate and colony-forming capacity of SCC9-fsc were remarkably decreased compared to those of SCC9-csc. Likewise, tumor size and volume of SCC9-fsc implanted into nude mice were also significantly inhibited with increases in the cell death index. Taken together, these results indicate that ω3-PUFAs induce apoptosis- and autophagy-associated cell death through ROS and Akt/mTOR signaling pathways in oral cancer cells. Thus, utilization of ω3-PUFAs may represent a promising therapeutic approach for chemoprevention and treatment of human oral cancer. [This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (No. 2011-0013263 and 2007-0054932).] Citation Format: Kyu Lim, Soyeon Shin, Tae-Hwa Hong, Kaipeng Jing, Soyeon Jeong, Soyeon Kim, Gi-Ryang Kweon, Seung-Kiel Park, Jong-Il Park. Omega-3 polyunsaturated fatty acids induce apoptotic and autophagic cell death through inhibition of Akt/mTOR pathway in human oral cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 5121. doi:10.1158/1538-7445.AM2014-5121
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-5121
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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    Abstract 862: Expression of the fat-1 gene retards the growth of cervical cancer cells in vitro and in vivo
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 862-862
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 862-862
    Abstract: Omega 3-polyunsaturated fatty acids (ω3-PUFAs) are known to inhibit proliferation of cancer cells; in contrast, ω6-PUFAs promote the growth of cancer cells. The fat-1 gene of the Caenorhabditis elegans encodes a ω3-desaturase that catalyzes the conversion ω6-PUFAs to ω3-PUFAs and then increases the amount of ω3-PUFAs. The objective of this study is to examine the effect of fat-1 gene expression on HeLa and SiHa human cervical cancer cells. Fat-1 gene stable cell lines (f-HeLa and f-SiHa) were established from HeLa and SiHa cells, respectively. The expression of fat-1 gene significantly inhibited cervical cancer cell proliferation and f-HeLa cells showed an increase in the proportion of cells in G2/M phase comparing with the cells expressing the control vector (c-HeLa). In addition, when treating HeLa cells with docosahexaenoic acid (DHA), an enhanced proportion of cells in the G2/M phase was also observed, indicating that fat-1 gene inhibited cervical cancer cell proliferation by inducing a G2/M phase cell-cycle arrest. Furthermore, transwell migration assay for invasion showed a reduction of cell migration in the f-HeLa cells when compared with the c-HeLa cells. Finally, the growth of f-HeLa cells in vivo was significantly reduced comparing with the c-HeLa cells when inoculated into nude mice. Taken together, these results suggest that the expression of fat-1 gene prevents cervical tumor growth and indicate a cancer therapeutic approach of the ω3-PUFAs. Therefore, a stable cell line of fat-1 gene is useful to study the anti-cancer effects of ω3-PUFAs. [This research was supproted by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (E00026 and R13-2007-020-01000-0)]. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 862. doi:10.1158/1538-7445.AM2011-862
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-862
    RVK:
    XA 36000
    RVK:
    XA 10000
    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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