• Proceedings of the Korean Society of Applied Pharmacology
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• 1997.04a
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• pp.101-101
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• 1997

As part of a drug discovery program to develope more effective platinum-based anticancer drugs, a series of platinum complexes trans -diaminocyclohexane platinum bi sdiphenylphosphino -ethane (KHPC-002) cis-diaminocyclohexane platinum bisdiphenylphosphino-ethane (KHPC-006) has been evaluated in vitro against 4 human carcinoma cell lines with those of cisplatin using a tetrazolium-based colorimetric assay (MTT assay). The cell lines were two human bladder carcinoma cell lines, HT-1197 and HT-1376, human colon carcinoma cell line, HCT-116, and prostate cancer cell line DU-145.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1997.04a
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• pp.111-111
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• 1997

As part of a drug discovery program to develope more effective platinum-based anticancer drugs, a series of platinum complexes trans-diaminocyclohexane platinum bi sdiphenylphosphino - ethane ( KHPC- 002) cis-diaminocyclohexane platinum bi sdiphenylphosphino - ethane ( KHPC- 006) has been evaluated in vitro against 4 human carcinoma cell lines with those of cisplatin using a tetrazolium-based colorimetric assay (MTT assay). The cell lines were two human bladder carcinoma cell lines, HT-1197 and HT-1376, human colon carcinoma cell line, HCT-116, and prostate cancer cell line DU-145. in vitro cytotoxic potential of each platinum complex was expressed as the cytotoxicity index (Cl, %).

• Journal of Ginseng Research
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• v.20 no.3
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• pp.219-225
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• 1996

This study was performed to investigate the inhibition mechanism of cancer cell proof iferation caused by the petroleum-ether extract of ginseng against human rectum (HRT-18), colon (HT-29), llepatoma (Hep G2) and prostate (LNCaP) cancer cells and monkey kidney cells (Vero 76). Cells were treated with the petroleum-ether extract of ginseng (50 to 200 $\mu\textrm{g}$/ml) in G1 or S phase of the cell cycle, and proliferation and protein kinase C activity were measured. The petroleum-eth or extract of ginseng inhibited proliferation of HRT-18, HT-29, Hep G2 and LNCaP when treated in Gl phase, but not in S phase. This result shows that the ginseng extract arrests the cell cycle in G1 phase, resulting in the inhibition of cell proliferation. At the same concentrations, treatment of the ginseng extract in G1 phase decreased protein kinase C activity, while the treatment in S phase had no effect. This reault suggests that protein kinase C might be involved in the inhibition of the cell cycle and proliferation of cancer cells caused by the petroleum-ether extract of ginseng.

• Journal of the Korean Applied Science and Technology
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• v.24 no.2
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• pp.109-116
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• 2007

2-Chlorobenzoyl hydrazine refluxed with benzoyl isothiocyanate and phenyl isothiocyanate in ethanol for 3 hours to give benzamide derivative (1) and anilinederivative (2) on yield of 71%and 95%, respectively. Benzamide derivative (1) reacted with ethanolic sodium hydroxide on reflux to afford cyclization product (3), followed by general substitution reaction of two steps to give acetamide (5), and derivatived acetamides 7a-7k, while aniline derivative (2) reacted with ethanolic sodium hydroxide on reflux to afford another cyclization product (4). Thiol (4) reacted with N-phenyl chloroacetamide in the presence of potassim carbonate to give acetamide derivative (6). Compounds 1-7kwere evaluated for their growth inhibition against five cancer cell lines, including human lung carcinoma (A-549), human prostate cancer (DU145), human colon adenocarcinoma (HT-29), human malignant melanoma (SK-MEL-2) and human ovary malignant ascites (SK-OV-3) with sulforhodamine B (SRB) assay. All compounds (1-7k) showed low inhibition activities under 50% on 100M concentration.

• Journal of Radiopharmaceuticals and Molecular Probes
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• v.4 no.2
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• pp.65-72
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• 2018

Prostate specific membrane antigen (PSMA) is a cell surface membrane protein, which is overexpressed in most prostate cancer. Recently, PET imaging with $[^{68}Ga]$PSMA-HBED-CC has been widely used for the diagnosis of recurrent prostate cancer and the studies on the diagnostic potential of $^{64}Cu$-labeled PSMA ligands reported actively. In this study, we monitored with biological evaluation in vivo and PET imaging of $^{64}Cu$-labeled PSMA ligand ($[^{64}Cu]$PSMA-617). The radiolabelling efficiency and stability of $[^{64}Cu]$PSMA-617 were confirmed by radio-thin layer chromatography. The radiolabeling efficiency of $[^{64}Cu]$PSMA-617 showed over 95%, and stabilities of intact remained over 98% in both human and mouse serum for 48 h. In normal male mice, in vivo uptake of $[^{64}Cu]$PSMA-617 in several organs was measured at 2, 4, 6, 24, 48 h after injection. Rapid blood clearance was observed for $[^{64}Cu]$PSMA-617. The high uptake was observed in the lung, liver, intestines and kidneys at 2 h postinjection, but was low in the other organs (1-2 %ID/g) at 4 h. The dynamic PET/CT images of 22RV1 tumor-bearing nude mice were acquired during 60 min and additionally acquired 24 h and 48 h after injection. In dynamic PET images, $[^{64}Cu]$PSMA-617 uptake ratio in tumors versus muscle was increased as time elaplsed until 60 minutes and remained in tumors at 48 h. In these results, the PET/CT imaging using $[^{64}Cu]$PSMA-617 in prostate cancer is expected to be useful for the diagnosis and treatment of prostate cancer patients.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.11
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• pp.5339-5343
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• 2012

The induction of apoptosis in target cells is a key mechanism for most anti-tumor therapies. Bufalin is a cardiotonic steroid that has the potential to induce differentiation and apoptosis of tumor cells. Research on bufalin has so far mainly involved leukemia, prostate cancer, gastric cancer and liver cancer, and has been confined to in vitro studies. The bufadienolides bufalin and cinobufagin have been shown to induce apoptosis in a wide spectrum of cancer cell. The present article reviews the anticancer effects of bufalin. It induces apoptosis of lung cancer cells via the PI3K/Akt pathway and also suppressed the proliferation of human non-small cell lung cancer A549 cell line in a time and dose dependent manner. Bufalin, bufotalin and gamabufotalin, key bufadienolides, significantly sensitize human breast cancer cells with differing ER-alpha status to apoptosis induction by the TNF-related apoptosis-inducing ligand (TRAIL). In addition, bufadienolides induce prostate cancer cell apoptosis more significantly than that in breast epithelial cell lines. Similar effects have been observed with hepatocellular carcinoma (HCC) but the detailed molecular mechanisms of inducing apoptosis in this case are still unclear. Bufalin exerts profound effects on leukemia therapy in vitro. Results of multiple studies indicate that bufalin has marked anti-tumor activities through its ability to induce apoptosis. Large-scale randomized, double-blind, placebo or positive drug parallel controlled studies are now required to confirm the efficacy and apoptosis-inducing potential of bufalin in various cancers in the cliniucal setting.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.11a
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• pp.165-165
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• 2004

• 한국약용작물학회:학술대회논문집
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• 2008.11a
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• pp.352-353
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• 2008

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.05a
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• pp.9-13
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• 2001

Genistein, a natural isoflavonoid phytoestrogen, is a strong inhibitor of protein tyrosine kinase and DNA topoisomerase II activities. Genistein has been shown to have anticancer proliferation, differentiation and chemopreventive effects. In the present study, we have addressed the mechanism of action by which genistein suppressed the proliferation of p53-null human prostate carcinoma cells.(omitted)

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.3
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• pp.1119-1122
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• 2016

Background: Punica granatum (PG) has been demonstrated to possess antitumor effects on various types of cancer cells. In this study, we determined antiproliferative properties of a seed extract of PG (PSE) from Iran in different human cancer cells. Materials and Methods: A methanolic extract of pomegranate seeds was prepared. Total phenolic content (TPC) and total flavonoid content (TFC) were assessed by colorimetric assays. Antioxidant activity was determined with reference to DPPH radical scavenging activity. The cytotoxicity of different doses of PSE (0, 5, 20, 100, 250, 500, $1000{\mu}g/ml$) was evaluated by MTT assays with A549 (lung non small cell carcinoma), MCF-7 (breast adenocarcinoma), SKOV3 (ovarian cancer cells), and PC-3 (prostate adenocarcinoma) cells. Results: Significant (P<0.01) or very significant (P<0.0001) differences were observed in comparison to negative controls at all tested doses ($5-1000{\mu}g/ml$). In all studied cancer cells, PSE reduced the cell viability to values below 23%, even at the lowest doses. In all cases, IC50 was determined at doses below $5{\mu}g/ml$. In this regard, SKOV3 ovarian cancer cells were the most responsive to antiproliferative effects of PSE with a maximum mean growth inhibition of 86.8% vs. 82.8%, 81.4% and 80.0% in MCF-7, PC-3 and A549 cells, respectively. Conclusions: Low doses of PSE exert potent antiproliferative effects on different human cancer cells SKOV3 ovarian cancer cells as most and A549 cells ar least responsive regarding cytotoxic effects. However, the mechanisms of action need to be addressed.