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Woong-Shick Ahn,Su-Mi Bae,Sun-Young Kwak,Ae Ju Lee,Aery Lee,Yong Seok Lee,Il-Ju Bae,Jin-Young Yoo,Young-Joo Lee,김종국,Hong-Seok Chang 대한암예방학회 2006 Journal of cancer prevention Vol.11 No.1
As2O3 has been reported to be effective for treating acute leukemia and induce apoptosis in many tumor cells. In this study, we evaluated the ability of a novel arsenical compound, As4O6, along with As2O3 to induce cell growth inhibition as well as apoptosis in human cervical cancer cells, SiHa cells in vitro. To examine the levels of apoptosis, SiHa cells were given two sensitive doses, 0.5 and 1μM of arsenical compounds, and then, DNA fragmentation assay and FACS analysis were conducted. In addition, Western blotting assay was done for the identification of target molecules for apoptosis. Both As2O3 and As4O6 caused dose-dependent inhibition of SiHa cell proliferation. In particular, As4O6 was more effective for suppressing SiHa cell growth, as compared to As2O3. In parallel with inhibition of cell proliferation, As4O6 caused an increase of the sub-G1 cell population significantly more than As2O3, as determined by propidium iodide DNA staining. This was confirmed by DNA fragmentation assay and annexin V staining. Western blotting analysis also showed that the proliferating cell nuclear antigen (PCNA) expression was suppressed by As4O6 significantly more than As2O3, and that Bcl-XL with sequence homology to Bcl-2 was significantly suppressed by As4O6. However, apoptosis-related proteins, p21 and Bax, were expressed by As4O6 significantly more than As2O3. Taken together, these findings suggest that a novel arsenic compound, As4O6 possesses more potent anti-proliferative effects on human cervical cancer cells with induction of apoptosis at least through activation in p21 and Bax proteins in vitro. (Cancer Prev Res 11, 39-45, 2006)
Targeted cellular process profiling approach for cervical cancer
안웅식 ( Woong Shick Ahn ),( Hyun Jung Kim ),( Il Young Kuk ),( Ho Chul Lee ),( Chung Mok Park ),( Hae Nam Kim ),( Duck Young Ro ),( Tae Chul Park ),( Jun Mo Lee ),( Sung Eun Namkoong ),( Chong Kook Kim 대한산부인과학회 2004 대한산부인과학회 학술대회 Vol.90 No.-
Neuroprotective Effects of Chronic Hesperetin Administration in Mice
Choi, Eon-Jeong,Ahn, Woong-Shick 대한약학회 2008 Archives of Pharmacal Research Vol.31 No.11
Flavonoids are considered therapeutic agents in neurodegenerative disease because of their neuroprotective activity. This study investigated the neuroprotective effects of hesperetin in the brains of mice administered hesperetin at 10 or 50 mg/kg body weight (BW) for five weeks. Hesperetin inhibited biomarkers of oxidative stress, such as the level of thiobarbituric acid-reactive substance (TBARS) and carbonyl content, although there was a significant reduction at the higher dose of hesperetin. Moreover, at the higher dose, hesperetin significantly activated the catalase and total superoxide dismutase (SOD) activities. The same patterns were observed in the protein expression, and the expression of CuZn-SOD was more pronounced than that of Mn-SOD. The reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio was increased significantly in a dose-dependent manner, as well as the glutathione peroxidase (GSH-px) and glutathione reductase (GR) activities. Moreover, hesperetin did not induce apoptosis, even at the higher dose, as evidenced by caspase-3 expression and its activity. Based on these results, hesperetin may have a neuroprotective effect via the inhibition of oxidative damage, together with activation of the antioxidant enzyme system.
Choi, Eun Jeong,Ahn, Woong Shick D.A. Spandidos 2009 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.23 No.2
<P>The present study was conducted to investigate the effects of dehydrocostuslactone on the cell cycle distribution and apoptosis of human ovarian cancer SK-OV-3 cells and explored the mechanisms underlying these effects. Dehydrocostuslactone significantly inhibited cell proliferation in a dose-dependent manner and produced significant cell cycle arrest at the G2/M interface when applied at its IC50 (10.7 microM) for this system. Under the same conditions, dehydrocostuslactone caused a slight decrease in the expression of the cell cycle regulatory proteins CDK4 and cyclin E, as well as a small increase in the expression of the cyclin-dependent kinase inhibitor p21Cip1. In addition, the dehydrocostuslactone-induced accumulation of cells at the G2/M phase transition interface resulted in a significant decrease in CDK1 together with cyclin A and cyclin B. This cell cycle arrest induced apoptosis, as confirmed by annexin V and DAPI staining. Following exposure to dehydrocostuslactone, there was a marked increase in the expression of the apoptotic protein Bax and the downstream target p53, a tumor suppressor transcription factor protein, causing the release of cytochrome c. Based on our findings, the mechanism by which dehydrocostuslactone causes cell cycle arrest is via CDK1 down-regulation, and its induction of apoptosis appears to be related to the activation of p53 and the release of cytochrome c.</P>