• Proceedings of the Korean Ceranic Society Conference
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• 2000.10a
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• pp.145.2-145
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• 2000

• Bulletin of the Korean Chemical Society
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• v.35 no.7
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• pp.2038-2042
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• 2014

4-(tert-Octyl)phenol derivatives bearing the D-mannitol substructure (6a, 6b, 7) were prepared from $\small{D}$-mannitol and evaluated their anticancer activity against human lung (A549) and prostate (Lncap, Du145, PC3) cancer cell lines. Among derivatives tested, the bis(tert-octyl)phenoxy compound 7 exhibited strongest proliferation inhibitory activities against human cancer cell lines tested, especially high sensitivity to human Du145 prostate cancer cells ($IC_{50}=7.3{\mu}M$).

• Proceedings of the Korean Society for Rock Mechanics Conference
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• 2009.03a
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• pp.145-150
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• 2009

• 대한방사선방어학회:학술대회논문집
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• 2009.04a
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• pp.144-145
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• 2009

• 대한핵의학회:학술대회논문집
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• 1991.05a
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• pp.144.2-145
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• 1991

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.1
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• pp.85-90
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• 2003

We investigated the effects of Oak smoke flavoring (OSF, Holyessing) on the growth of DU145 and PC-3 human prostate carcinoma cells. OSF treatment resulted in a concentration-dependent growth inhibition in both DU145 and PC3 cell lines. The anti-proliferative effect of OSF treatment was associated with the induction of apoptotic cell death which was confirmed by morphological change such as membrane shrinking, rounding up and chromatin condensation in DU145 and PC-3 cells. DNA flow cytometry analysis confirmed that OSF treatment increased population of apoptotic sub-G1 phase. Furthermore, we observed an increase of pro-apoptotic protein Bax expression and a decrease of anti-apoptotic protein Bcl-2 by OSF treatment in a dose-dependent manner. OSF also induced a proteolytic cleavage of specific target proteins such as poly(ADP-ribose) polymerase (PARP) and β-catenin proteins. The present results indicated that OSF-induced inhibition of human prostate carcinoma cell proliferation is associated with the induction of apoptosis.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.6
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• pp.1661-1665
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• 2004

Herba Patriniae(HP) has been known to exert anti-tumoral activity in Korea. However, its molecular mechanism, of action is not understood. In this study, we found that HP induced apoptosis in androgen-dependent prostate cancer DU145 cells as evidenced by DNA fragmentation and chromatine condensation in hoechst dye staining. Our data demonstrated that HP-induced apoptotic cell death was accompanied by activation of caspase-3 and cleavages of its substrates, poly(ADP-ribose) polymerase(PARP) in a time- and concentration-dependent manner. Taken together, these results suggest that HP induces the activation of caspase-3, degradation of PARP, and eventually leads to apoptotic cell death.

• Toxicological Research
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• v.19 no.2
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• pp.91-98
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• 2003

Alkylating agents form alkylated base adducts in the DNA and cause DNA lesions leading to cell killing. In this study, we investigated the mechanism of apoptosis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in PC-3 and DU145 human prostate carcinoma cell lines. MNNG treatment resulted in the inhibition of cell proliferation in a concentration-dependent manner to a similar extent in both cell lines. This anti-proliferative effect of PC-3 and DU145 cells by MNNG was associated with morphological changed such as membrane shrinking, cell rounding up and formation of apoptotic bodies. MNNG treatment also induced a proteolytic cleavage of specific target proteins such as poly(ADP-ribose) polymerase (PARP) and $\beta$-catenin proteins in DU145 cells but in PC-3 cells. Furthermore, we observed an increase of proapoptotic protein Bax family expression and a decrease of antiapoptotic protein Bcl-2 family by MNNG treatment in a concentration-dependent manner MNNG also induced a proteolytic activation of caspase-3 and -9, which is believed to play a central role in the apoptotic signaling pathway.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.4
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• pp.1639-1644
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• 2012

The aim of this study was to investigate the expression and significance of microsomal prostaglandin synthase-1 (mPGES-1) and Beclin-1 in the development of prostate cancer (PCa). Immunohistochemistry was performed on paraffin-embedded sections with rabbit polyclonal against mPGES-1 and Beclin-1 in 40 PCa, 40 benign prostatic hyperplasia (BPH) and 10 normal prostate specimens for this purpose. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied for mRNA expression of mPGES-1 and Beclin-1, while MTT assays were used to ascertain the best working concentration of the mPGES-1 inhibitor (CAY10526). The effect of CAY10526 treatment on expression of Beclin-1 in DU-145 cells was studied using Western blot analysis. Localization of Beclin-1 and mPGES-1 was in endochylema. Significant differences in expression was noted among PCa, BPH and normal issues (P<0.05). Beclin-1 expression inversely correlated with mPGES-1 expression in PCa tissue (P<0.05). CAY10526 could significantly block mPGES-1 expression and the proliferation of DU-145 cells (P<0.05), while increasing Beclin-1 levels (P<0.05). Overexpression of mPGES-1 could decrease the autophagic PCa cell death. Inhibiting the expression of mPGES-1 may lead to DU-145 cell death and up-regulation of Beclin-1. The results suggest that inhibition of mPGES-1 may have therapeutic potential for PCa in the future.

• Biomolecules & Therapeutics
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• v.23 no.5
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• pp.434-441
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• 2015

Histone deacetylase (HDAC) inhibitors are considered novel agents for cancer chemotherapy. We previously investigated MHY219, a new HDAC inhibitor, and its potent anticancer activity in human prostate cancer cells. In the present study, we evaluated MHY219 molecular mechanisms involved in the regulation of prostate cancer cell migration. Similar to suberanilohydroxamic acid (SAHA), MHY219 inhibited HDAC1 enzyme activity in a dose-dependent manner. MHY219 cytotoxicity was higher in LNCaP ($IC_{50}=0.67{\mu}M$) than in DU145 cells ($IC_{50}=1.10{\mu}M$) and PC3 cells ($IC_{50}=5.60{\mu}M$) after 48 h of treatment. MHY219 significantly inhibited the HDAC1 protein levels in LNCaP and DU145 cells at high concentrations. However, inhibitory effects of MHY219 on HDAC proteins levels varied based on the cell type. MHY219 significantly inhibited LNCaP and DU145 cells migration by down-regulation of matrix metalloprotease-1 (MMP-1) and MMP-2 and induction of tissue inhibitor of metalloproteinases-1 (TIMP-1). These results suggest that MHY219 may potentially be used as an anticancer agent to block cancer cell migration through the repression of MMP-1 and MMP-2, which is related to the reduction of HDAC1.