• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2003.10a
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• pp.189-189
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• 2003

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.11a
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• pp.116-116
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• 2004

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.189-189
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• 2003

Recent studies suggest that inflammatory events are implicated in a variety of human diseases including cancer and neurodegenerative diseases. It has been reported that expression of inducible cyclooxygenase (COX) and nitric oxide (NO) synthase and subsequent production of prostaglandins (PG)s and NO, respectively are elevated in many inflammatory disorders.(omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.153.1-153.1
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• 2003

Oxidative stress induced by reactive oxygen intermediates (ROIs) has been implicated in a variety of human diseases including cancer, diabetes, rheumatoid arthritis and neurodegenerative disorders. Hydrogen peroxide ($H_2O_2$), a representative ROI which is produced during the cellular redox process, can cause cell death via apoptosis and/or necrosis depending on its concentrations. l5-Deoxy-$D^{12, 14}$ prostaglandin $J_2$ (15d-$PGJ_2$), a dehydration product of prostaglandin $D_2$, has been reportd to possess a number of biological activities such as anti-inflammatory, anticarcinogenic, and antioxidative properties. (omitted)

• Korean Journal of Veterinary Research
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• v.27 no.2
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• pp.185-189
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• 1987

The number of splenic lymphocyte, serum prostaglandin $E_2$ level and natural killer cell activity were assayed after single whole body irradiation of a sublethal dose of $^{60}Co-{\gamma}$ ray to C57BL/6J mice. With a view to knowing the relationships between radiation induced prostaglandin $E_2$ level and the normal natural killer cell activity after natural killer cell-target cell conjugation, The change of normal natural killer cell activity were measured by administration of prostaglandin $E_2$ containing serum from irradiated mice. The results were summarized as follows; 1. The total number of splenic lymphocyte was significantly decreased by irradiation and the number was not affected by indometacin, prostaglandin synthesis inhibitor, treatment. 2. Serum prostaglandin $E_2$ level was increased in irradiated mice, but indometacin treated mice group showed low level of prostaglandin $E_2$. 3. In the case of irradiated mice, natural killer cell activity was not shown any difference between irradiated group and indometacin combined group. But when natural killer cell-target cell conjugations were exposed to the serum of each group during cytotoxic activity assay, whereas the normal natural killer cell activity was significantly decreased by treatment of serum from irradiated mice, the activity was not changed by treatment of indometacin pretreated mice serum. This result indicated that the prostaglandin $E_2$ induced by the radiation inhibited the post-target binding cytolytic process of natural killer activity.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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• pp.110-110
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• 2002

15-Deoxy-$\Delta$12, 14-prostaglandin J2 (15-deoxy-PGJ2), a naturally occurring ligand activates the peroxisome proliferator-activated receptor-$\gamma$(PPAR-$\gamma$). It was known to have promoting ability of nerve growth factor(NGF)-induced neurite extension. However, it is not clear yet as to what signaling pathway is involved in its promoting ability of neurite extension.(omitted)

• Proceedings of the PSK Conference
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• 2000.10a
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• pp.256.2-257
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• 2000

• Journal of the korean veterinary medical association
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• v.14 no.3
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• pp.153-156
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• 1978

Therapeutic effects of synthetic PGF 2 alpha (Estrumate, ICI) were evaluated in various cases of bovine infertility. of 19 anestrus dairy cows (Holstein-Friesian) for 3 to 12 months post-partum, 16 showed estrus within 10 days after a single intramuscular

• Proceedings of the PSK Conference
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• 2001.04a
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• pp.236.2-237
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• 2001

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.11
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• pp.6761-6767
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• 2013

The nuclear receptor, peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$), is expressed in various cancer cells including breast, prostate, colorectal and cervical examples. An endogenous ligand of $PPAR{\gamma}$, 15-deoxy-${\Delta}^{12,14}$ prostaglandin $J_2$ (PGJ2), is emerging as a potent anticancer agent but the exact mechanism has not been fully elucidated, especially in breast cancer. The present study compared the anticancer effects of PGJ2 on estrogen receptor alpha ($ER{\alpha}$)-positive (MCF-7) and $ER{\alpha}$-negative (MDA-MB-231) human breast cancer cells. Based on the reported signalling cross-talk between $ER{\alpha}$ and $ER{\alpha}$, the effect of the $ER{\alpha}$ ligand, $17{\beta}$-estradiol (E2) on the anticancer activities of PGJ2 in both types of cells was also explored. Here we report that PGJ2 inhibited proliferation of both MCF-7 and MDA-MB-231 cells by inducing apoptotic cell death with active involvement of mitochondria. The presence of E2 potentiated PGJ2-induced apoptosis in MCF-7, but not in MDA-MB-231 cells. The $ER{\alpha}$ antagonist, GW9662, failed to block PGJ2-induced activities but potentiated its effects in MCF-7 cells, instead. Interestingly, GW9662 also proved capable of inducing apoptotic cell death. It can be concluded that E2 enhances $ER{\alpha}$-independent anticancer effects of PGJ2 in the presence of its receptor.