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  • 1
    Online Resource
    Online Resource
    Apicularen A Induces Cell Death through Fas Ligand Up-Regulation and Microtubule Disruption by Tubulin Down-Regulation in HM7 Human Colon Cancer Cells
    American Association for Cancer Research (AACR) ; 2007
    In:  Clinical Cancer Research Vol. 13, No. 21 ( 2007-11-01), p. 6509-6517
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 13, No. 21 ( 2007-11-01), p. 6509-6517
    Abstract: Purpose: Apicularen A has been shown to cause growth inhibition and apoptosis in several cancer cell lines. However, the mechanisms of apicularen A–induced cell death and in vivo effects remain unclear. In this study, we investigated the molecular mechanisms of apicularen A–induced cell death in HM7 human colon cancer cells in vitro and anticancer activity in vivo. Experimental Design: We tested cytotoxicity with a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, apoptosis with DNA fragmentation assay, mitochondrial membrane potential, and cell cycle with fluorescence-activated cell sorting. Caspase activation was done by fluorometry. Alterations of microtubule structure, tubulin protein, and mRNA level were assessed by immunofluorescence, Western blot, and reverse transcription-PCR. In vivo studies were assessed using nude mice tumor cell growth in xenograft model and liver colonization assay. Results: Apicularen A treatment of HM7 cells inhibited cell growth and this inhibition was partially rescued by z-VAD-fmk. Apicularen A caused accumulation of sub-G1-G0, DNA fragmentation, Fas ligand induction, and activation of caspase-8 and caspase-3, but mitochondrial membrane potential was not changed. Furthermore, β-tubulin protein and mRNA were decreased by apicularen A, but in vitro polymerization of tubulin was not affected. Concurrently, apicularen A–treated cell showed disruption of microtubule architecture. In in vivo studies, apicularen A reduced tumor volume by ∼72% at the end of a 15-day treatment. Moreover, apicularen A reduced liver colonization as much as 95.6% (50 μg/kg/d). Conclusion: Apicularen A induces cell death of HM7 cells through up-regulating Fas ligand and disruption of microtubule architecture with down-regulation of tubulin level. These findings indicate that apicularen A is a promising new microtubule-targeting compound.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-07-1428
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2007
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    detail.hit.zdb_id: 2036787-9
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  • 2
    Online Resource
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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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  • 3
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    Abstract 4654: Docosahexaenoic acid induces autophagy through reactive oxygen species /mTOR pathway in p53 mutant cancer cells
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 4654-4654
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 4654-4654
    Abstract: Our previous studies reported that docosahexaenoic acid (DHA) induces autophagy through p53 inhibition in the wild-type p53 cancer cells. This study attempts to elucidate the molecular mechanism underlying DHA-induced autophagy in PC3 and DU145 prostate cancer cells harboring mutant p53. DHA increased both the level of microtubule-associated protein light-chain 3 (LC3) and the number of autophagic vacuoles. Autophagic flux assay confirmed that DHA-induced increase in LC3-II and autophagic vesicles was an outcome of autophagic process activation, indicating that DHA also induces autophagy in p53 mutant cancer cells. DHA treatment also increased the level of reactive oxygen species (ROS) as measured by dihydroethidine staining, and pretreatment of an antioxidant, N-acetylcysteine (NAC), significantly inhibited the ROS production as well as autophagy induced by DHA, suggesting that ROS regulates the autophagic process triggered by DHA. Further experiments showed that the mechanism of DHA-induced autophagy associated with ROS production was related to a decrease in the activity of mammalian target of rapamycin (mTOR). NAC remarkably restored the decreases in the levels of phospho-mTOR and 4EBP, an mTOR downstream molecule, induced by DHA as analyzed by the Western blot assay. Furthermore, the level of phospho-AMPK, which negatively regulates mTOR was increased, while phospho-Akt was reduced during the DHA-induced autophagy, indicating the involvement of AMPK and Akt signalings. Collectively, our results demonstrate that DHA induces autophagy through the ROS-mediated mTOR inactivation in p53 mutant prostate cancer cells. This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (No. 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 4654. doi:1538-7445.AM2012-4654
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-4654
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 4
    Online Resource
    Online Resource
    Omega-3-Polyunsaturated Fatty Acids Suppress Pancreatic Cancer Cell Growth in vitro and in vivo via Downregulation of Wnt/Beta-Catenin Signaling
    Elsevier BV ; 2011
    In:  Pancreatology Vol. 11, No. 6 ( 2011-12), p. 574-584
    Details
    In: Pancreatology, Elsevier BV, Vol. 11, No. 6 ( 2011-12), p. 574-584
    Type of Medium: Online Resource
    ISSN: 1424-3903
    URL: Article
    DOI: 10.1159/000334468
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2011
    detail.hit.zdb_id: 2043694-4
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  • 5
    Online Resource
    Online Resource
    Expression regulation and function of Pref-1 during adipogenesis of human mesenchymal stem cells (MSCs)
    Elsevier BV ; 2009
    In:  Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids Vol. 1791, No. 8 ( 2009-8), p. 816-826
    Details
    In: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, Elsevier BV, Vol. 1791, No. 8 ( 2009-8), p. 816-826
    Type of Medium: Online Resource
    ISSN: 1388-1981
    URL: Article
    DOI: 10.1016/j.bbalip.2009.04.010
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2009
    detail.hit.zdb_id: 2209502-0
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Docosahexaenoic acid induces autophagy through p53/AMPK/mTOR signaling and promotes apoptosis in human cancer cells harboring wild-type p53
    Informa UK Limited ; 2011
    In:  Autophagy Vol. 7, No. 11 ( 2011-11), p. 1348-1358
    Details
    In: Autophagy, Informa UK Limited, Vol. 7, No. 11 ( 2011-11), p. 1348-1358
    Type of Medium: Online Resource
    ISSN: 1554-8627 , 1554-8635
    URL: Article
    DOI: 10.4161/auto.7.11.16658
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2011
    detail.hit.zdb_id: 2262043-6
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Abstract 4175: Reactive oxygen species-dependent ERK and JNK activation is important to docasahexaenoic acid-induced cell cytotoxicity in human ovarian cancer cells
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 4175-4175
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 4175-4175
    Abstract: Although abundant experimental evidences show that the Omega-3 polyunsaturated fatty acids (≥3-PUFAs) prevent carcinogenesis, the exact molecular mechanisms of the anti-cancer actions of α3-PUFAs in ovarian cancer remain incompletely understood. In the present study, the effectiveness of docosahexaenoic acid (DHA), a α3-PUFA, against ovarian cancer cells was investigated. We found that DHA induced cell cytotoxicity in three ovarian cancer cells including PA-1, MDAH2774 and ID8. DHA treatment inhibited the cell proliferation of PA-1 cells in a dose- and time-dependent manner. Meanwhile, DHA-treated ovarian cancer cells showed increased levels of caspase-3 activity, Annexin-V staining positive cells, TUNEL-positive cells and the portion of sub-G1 cells, suggesting that DHA-induced cell death is mainly associated with apoptosis. Western blot and immunocytochemistry assays revealed that DHA also remarkably increased the levels of phospho-ERK and phospho-JNK in both cytosol and nucleus. Moreover, knockdown ERK and JNK by small interfering RNAs partially attenuated the apoptosis induced by DHA, indicating that ERK and JNK activation is responsible for the apoptosis in DHA-treated ovarian cancer cells. In addition, we determined that the activation of ERK and JNK was associated with the reactive oxygen species (ROS) production induced by DHA. ROS scavenger, N-acetyl-L-cysteine (NAC), almost completely blocked the ERK and JNK phosphorylation as well as the apoptosis triggered by DHA. Together, these results indicate that DHA induces ROS and the ROS-dependent ERK and JNK activation is important to DHA-induced cell cytotoxicity in human ovarian cancer cells. [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 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 4175. doi:1538-7445.AM2012-4175
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-4175
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 8
    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
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 9
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    Online Resource
    Abstract 4457: Omega-3 polyunsaturated fatty acids induce apoptosis cell death and inhibit LPS-induced invasion in PC3 cells
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 4457-4457
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 4457-4457
    Abstract: Dietary fat as a potential risk factor for cancer has been the focus of many epidemiologic and basic researchers, but the findings have been inconclusive. Toll-like receptor 4 (TLR4)-mediated signaling has been implicated in tumor cell invasion, survival, and metastasis in a variety of cancers. In this study, we have investigated anticancer action of ω3-PUFAs and effect of ω3-PUFAs on LPS-mediated TLR4 signaling in prostate cancer. DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid) treatment resulted in a dose-dependent reduction of cell viability with apoptosis of PC3 cells as confirmed by TUNEL assay. In contrast, AA (arachidonic acid), a ω6-PUFA, exhibited no significant effect. Moreover, invasiveness of PC3 cells was inhibited in a dose-dependent manner by treatment of DHA, while AA showed no significant effect. In zymography, MMP-2 activity was inhibited by DHA treatment and MMP-9 and MMP-2 promoter activities were also inhibited. DHA inhibited Cox-2 and VEGF promoter activities and NF-kB reporter activity was also decreased. The expression of TLR4 was confirmed by RT-PCR in PC3 cells and DHA dramatically inhibited the LPS-induced invasion of PC3 cells. In in vivo experiments, when mouse prostate cancer cells (RM1) were injected into the tail vein of Fat1 mice (Fat1 transgenic mice express a Caenorhabditis elegans ω3-desaturase converting ω6- to ω3-PUFAs endogenously.) and WT (wild type mice), lung metastasis was significantly inhibited in Fat1 transgenic mice compared to WT mice. In conclusion, the present study suggests that ω3-PUFAs may inhibit prostate cancer cell growth, and invasion through decrease of MMPs, Cox-2, VEGF and NF-kB reporter activities. Moreover LPS-mediated invasiveness was inhibited by DHA. These findings provide important preclinical evidence and molecular insight for utilization of ω-3 PUFAs for the chemoprevention and treatment of human prostate cancer. [This work was supported by the Korea Science and Engineering Foundation (KOSEF) grant funded by the Infection Signaling Network Research Center (R13-2007-020-01000-0) at Chungnam National University]. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4457.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-4457
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 10
    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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