• Asian Pacific Journal of Cancer Prevention
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• v.15 no.24
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• pp.10613-10619
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• 2015

Background: Both alcohol and aqueous extracts of Sauromatum giganteum(Engl.) Cusimano and Hett, the dried root tuber of which is named Baifuzi in Chinese, have been used for folklore treatment of cancer in Northeast of China. However, little is known about which is most suitable to the cancer therapy. Materials and Methods: Serum pharmacology and MTT assays were adopted to detect the effects of ethanol and aqueous extracts of Sauromatum giganteum(Engl.) Cusimano and Hett, prepared by heat reflux methods, on proliferation of different cancer cells. Results: Cancer cells treated with medium supplemented with 10%, 20%, 40% serum(v/v) containing ethanol extract had a decline in viability, with inhibition rates of 7.69%, 21.8%, 41.9% in MCF-7 cells, 42.8%, 48.1%, 51.8% in SGC-7901 cells, 44.1%, 49.2%, 53.7% in SMMC-7721 cells, 6.8%, 15.2%, 39.8% in HepG2 cells, 7.57%, 16.3%, 36.2% in HeLa cells, 6.24%, 12.5%, 27.4% in A549 cells, and 7.20%, 17.5%, 31.3% in MDA-MB-231 cells, respectively. Viability in the aqueous extract groups was no different with that of controls. Conclusions: An ethanol extract of Sauromatum giganteum(Engl.) Cusimano and Hett inhibited the proliferation of SMMC-7721, SGC-7901 and MCF-7 cells, which supports the use of alcoholic but not aqueous extracts for control of sensive cancers, which might include hepatocarcinoma, gastric cancer and breast cancer.

• YAKHAK HOEJI
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• v.35 no.3
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• pp.203-215
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• 1991

Using the calorimetric [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] (MTT)assay, we evaluated the chemosensitivity of 8 anticancer drugs{vincristine(VCR), vinblastine(VBL), adriamycin(ADR), cisplatin(CPDD), etoposide(VP-16), cytosine arabinoside(ara-C), bleomycin (Bleo) and cyclophosphamide(CYC)} and the cytotoxicity-enhancing effects of ($\pm$)-ar-turmerone and the extracts of the crude drugs {Lithospermum eythrorhizon(LE) and Scutellaria baicalensis (SB)} on the above mentioned anticancer drugs against HL-60 and KG-1 cells among 8 anticancer drugs, VCR, VBL, ADR, and CPDD inhibited the growth of both cell lines by more than 50%, while VP-16, ara-C, Bleo, and CYC were less effective. ($\pm$)-ar-Turmerone had significant inhibitory effects against both cell lines, showing the ID$_{50}$ values of 11.730 $\mu\textrm{g}$/ml and 0.292 $\mu\textrm{g}$/ml for HL-60 and KG-1 cells. respectively. But the extracts of LE and SB roots showed no significant cytotoxic effects. According to ID$_{50}$ values, the cytotoxicities of VCR, VBL and ADR against HL-60 were enhanced two, eight and three times by mixing ($\pm$)-ar-turmerone, five, seven and three times by adding the extract of LE root, and twenty, six and three times by mixing the extract of SB root, respectively. The cytotoxicities of the above mentioned drugs against KG-1 cell were enhanced two, seven and three times by mixing ($\pm$)-ar-turmerone, two, three and three times by combining wilth the extract of LB root, and two, five and two times by adding the extract of SB root, respectively. The cytotoxicity-potentiating effects of ($\pm$)-ar-turmerone and the extracts of LE and SB roots against HL-60 cell were greater than KG-1 cell.

• Journal of Environmental Health Sciences
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• v.21 no.3
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• pp.67-76
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• 1995

The frequencies of chromosome aberrations and sister chromatid-exchanges in peripheral blood lymphocyte of 44 nurses handling anticancer drugs were compared with those in 44 age-match controls. The frequencies of dicentric chrdmosome were $2.4\times 10^{-3}$ in the exposed and $0.5\times 10^{-3}$ in the control. The frequencies of sister cromatid exchanges in the exposed were slightly higher (5.68 SCEs/cell) than those in the control (5.04 SCEs/cell). The frequencies of chromosome aberrations and sister cromatid exchanges were not associated with duration of drug handling and types of anticancer drugs, but associated with use of safety cover.

• BMB Reports
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• v.49 no.4
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• pp.238-243
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• 2016

The efficacy of anticancer drugs depends on a variety of signaling pathways, which can be positively or negatively regulated. In this study, we show that SETDB1 HMTase is down-regulated at the transcriptional level by several anticancer drugs, due to its inherent instability. Using RNA sequence analysis, we identified FosB as being regulated by SETDB1 during anticancer drug therapy. FosB expression was increased by treatment with doxorubicin, taxol and siSETDB1. Moreover, FosB was associated with an increased rate of proliferation. Combinatory transfection of siFosB and siSETDB1 was slightly increased compared to transfection of siFosB. Furthermore, FosB was regulated by multiple kinase pathways. ChIP analysis showed that SETDB1 and H3K9me3 interact with a specific region of the FosB promoter. These results suggest that SETDB1-mediated FosB expression is a common molecular phenomenon, and might be a novel pathway responsible for the increase in cell proliferation that frequently occurs during anticancer drug therapy.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2000.04a
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• pp.8-9
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• 2000

Despite the advances made in the past few decades in cancer chemotherapy, many conventional anticancer drugs display relatively poor selectivity for cancer cells. The nonselectivity of anticancer drugs and the development of anticancer drug resistance have been recognized as serious limitations in their clinical usefulness. Therefore, a major challenge in cancer chemotherapy is the development of new anticancer agents with improved selectivity for tumor cells as well as the prevention of the host cell resistance, both of which result in the improvement of therapeutic effect against cancer cells. Cyclophosphamide (CP), a widely used anticancer agent, is a prodrug that is activated by hepatic microsomal mixed-function oxidase (MFO) catalyzed C$_4$- hydroxylation. The resulting 4-hydroxycyclophosphamide (4-OH-CP) is converted to the ring-opened tautomer to aldophosphamide (Aldo) which subsequently undergoes a base- catalyzed ${\beta}$-elimination to generate cytotoxic phosphoramide mustard (PDA) and acrolein. The cytotoxic activity of CP is attributed to the aziridinium ion species derived from PDA that cross-links interstrand DNA.

• Journal of Haehwa Medicine
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• v.3 no.2
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• pp.315-321
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• 1995

An extensive anticancer drug screening from natural resources has been carried out primarily using murine tumor model for past fourty years. Recently a new screening program from NCI, so called disease-oriented screening system. has been estabished to detect anticancer drugs that show selective growth inhibition toward variety of tissue specific human solid tumors originated from leukemia, lung, colon, CNS, melanoma, ovarian, renal, prostate amd breast. To develope the anticancer drugs from oriental medicinal herbs, we investigated the cytotoxic effects against human tumor cell panels with 23 kinds of MeOH extract of medicinal herbs. Evodiae Fructus, Meliae Toosendan Fructus, Saussureae Radix and Pharbitidis Semen showed strong activities against several tumor cell lines.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.15
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• pp.6437-6441
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• 2014

Background: Oridonin isolated from Rabdosia rubescens, a plant used to treat cancer in Chinese folk medicine, is one of the most important antitumor active ingredients. Previous studies have shown that oridonin has antitumor activities in vivo and in vitro, but little is known about cell cycle effects of oridonin in gastric cancer. Materials and Methods: MTT assay was adopted to detect the proliferation inhibition of SGC-7901 cells, the cell cycle was assessed by flow cytometry and protein expression by Western blotting. Results: Oridonin could inhibit SGC-7901 cell proliferation, the $IC_{50}$ being $15.6{\mu}M$, and blocked SGC-7901 cell cycling in the $G_2/M$ phase. The agent also decreased the protein expression of cyclinB1 and CDK1. Conclusions: Oridonin may inhibit SGC-7901 growth and block the cells in the $G_2/M$ phase by decreasing Cdk1 and cyclinB1 proteins.

• Molecular & Cellular Toxicology
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• v.1 no.4
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• pp.248-255
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• 2005

To understand the response of cancer cells to anticancer drugs at the gene expression level, we examined the gene expression changes in response to five anticancer drugs, 5-fluorouracil, cytarabine, cisplatin, paclitaxel, and cytochalasin D in NCI-H460 human lung cancer cells. Of the five drugs, 5-fluorouracil had the most distinctive gene expression signature. By clustering genes whose expression changed significantly, we identified three clusters with unique gene expression patterns. The first cluster reflected the up-regulation of gene expression by cisplatin, and included genes involved in cell death and DNA repair. The second cluster pointed to a general reduction of gene expression by most of the anticancer drugs tested. A number of genes in this cluster are involved in signal transduction that is important for communication between cells and reception of extracellular signals. The last cluster represented reduced gene expression in response to 5-fluorouracil, the genes involved being implicated in DNA metabolism, the cell cycle, and RNA processing. Since the gene expression signature of 5-fluorouracil was unique, we investigated it in more detail. Significance analysis of microarray data (SAM) identified 808 genes whose expression was significantly altered by 5-fluorouracil. Among the up-regulated genes, those affecting apoptosis were the most noteworthy. The down-regulated genes were mainly associated with transcription-and translation-related processes which are known targets of 5-fluorouracil. These results suggest that the gene expression signature of an anticancer drug is closely related to its physiological action and the response of caner cells.

• Proceedings of the Materials Research Society of Korea Conference
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• 2011.05a
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• pp.52.2-52.2
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• 2011

Flat form technology for constructing anticancer loaded multi-walled carbon nanotubes (mwCNTs) was introduced in this study. Conventional anticancer drugs, such as MTX (Methotrexate), cisplatin, DOX (Doxorubicin hydrochloride), DAU (Daunorubicin) and EPI (epirubicin) were bio-conjugated with folic acid (FA) for selective targeting tumor cells. Loading efficiencies of the used anticancer drugs on mwCNTs have shown different order of bindings depending on the molecular bind affinity of NH (amine) formation on mwCNTs. MTT assays have shown increased selective target efficiency of FA conjugated mwCNTs on breast cancer cell growth inhibition. All results collectively indicated promising application of mwCNTs as a smart inorganic nanomaterial for selective targeting drug delivery vehicle at tumor tissues.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1995.04a
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• pp.124-124
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• 1995

Cisplatinum is often effective in cancer treatment, but potent nephrotoxicity limits its clinical use. We have, therefore, developed new anticancer drugs that contain platinum. We have synthesized six new platinum compounds based on Figure 1. Drugs were initially administrated at 5${\times}$10$\^$-4/M with 48 hours exposure in monolayer cultures of primary rabbit proximal tubular cells and human renal cortical cells with the M.T.T. endpoint to measure toxicity. Drug concentrations of 10$\^$-3/M, 10$\^$-4/M, and 10$\^$-5/M with 72 hours exposure were used for human renal cortical tissues in 7 weeks histoculture with toxicity measured by the glucose-consumption endpoint. From these studies, we determined that the new platinum drugs have lower nephrotoxicity than cisplatinum. Drugs D, E, and H. have lower nephrotoxicity than the other new drugs. We are currently measuring the anticancer efficacy of drugs D, E, and H.