• Journal of Korean society of Dental Hygiene
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• v.14 no.4
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• pp.601-608
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• 2014

Objectives : The purpose of the study is to examine the apoptotic effects of Pseudomonas aeruginosa exotoxin A(PEA) in squamous cell carcinoma(SCC) 25 cells. Methods : Cell growth reduction and apoptosis induced by PEA were confirmed by WST-1 assay, Hoechst 33258 staining, flow cytometry analysis, and Western blot assay. Results : The PEA treatment decreased the cell viability in a dose and time dependent manner: control; $100{\pm}0^e$(p<0.01), 0.1875 nM; $87{\pm}4.36^d$(p<0.01), 0.375 nM; $82{\pm}0.58^d$(p<0.01), 0.75 nM; $72{\pm}1.67^c$(p<0.01), 1.5 nM; $51{\pm}1.53^{bc}$(p<0.01), 7.5 nM; $31{\pm}1.20^{ab}$(p<0.01), 15 nM; $26{\pm}0.67^a$(p<0.01), control; $100{\pm}0^a$(p<0.05), 24 h; $51{\pm}1.53^b$(p<0.05), 48 h; $16{\pm}0.5^c$(p<0.05), 72 h; $12{\pm}1.67^d$%(p<0.05). The PEA was observed on SCC 25 cells with the half maximal inhibitory concentration(IC50) value of 1.5 nM at 24 hours. The PEA treated SCC 25 cells demonstrated several types of apoptotic indications, such as nuclear condensation, the increase of sub G1, and the cleavage of PARP-1 and DFF 45. Conclusions : PEA showed anti-cancer activity against SCC 25 cells via apoptosis. PEA may potentially contribute to human oral cancer treatment.

• Journal of Ginseng Research
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• v.39 no.2
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• pp.125-134
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• 2015

Background: Black ginseng (Ginseng Radix nigra, BG) refers to the ginseng steamed for nine times and fine roots (hairy roots) of that is called fine black ginseng (FBG). It is known that the content of saponin of FBG is higher than that of BG. Therefore, in this study, we examined antitumor effects against MCF-7 breast cancer cells to target the FBG extract and its main component, ginsenoside Rg5 (Rg5). Methods: Action mechanism was determined by MTT assay, cell cycle assay and western blot analysis. Results: The results from MTT assay showed that MCF-7 cell proliferation was inhibited by Rg5 treatment for 24, 48 and 72 h in a dose-dependent manner. Rg5 at different concentrations (0, 25, 50 and $100{\mu}M$), induced cell cycle arrest in G0/G1 phase through regulation of cell cycle-related proteins in MCF-7 cells. As shown in the results from western blot analysis, Rg5 increased expression of p53, $p21^{WAF1/CIP1}$ and $p15^{INK4B}$ and decreased expression of Cyclin D1, Cyclin E2 and CDK4. Expression of apoptosiserelated proteins including Bax, PARP and Cytochrome c was also regulated by Rg5. These results indicate that Rg5 stimulated cell apoptosis and cell cycle arrest at G0/G1 phase via regulation of cell cycle-associated proteins in MCF-7 cells. Conclusion: Rg5 promotes breast cancer cell apoptosis in a multi-path manner with higher potency compared to 20(S)-ginsenoside Rg3 (Rg3) in MCF-7 (HER2/ER+) and MDA-MB-453 (HER2+/ER) human breast cancer cell lines, and this suggests that Rg5 might be an effective natural new material in improving breast cancer.

• Journal of Acupuncture Research
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• v.22 no.3
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• pp.169-183
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• 2005

Objective : The purpose of this study was to investigate the anti-caner effect of cobrotoxin on the prostatic cancer cell line (PC-3).The goal of study is to ascertain whether cobrotoxin inhibits tile cell growth and cell cycle of PC-3, or the expression of relative genes and whether the regression of PC-3 cell growth is due to cell death or the expression of gene related to apoptosis. Methods : After the treatment of Pc-3 cells with cobrotoxin, we performed 형광현미경, MTT assay, Western blotting, Flow cytometry, PAGE electrophoresis and Surface plasmon resonance analysis to identify the cell viability, cell death, apoptosis, the changes of cell cycle and the related protein, Adk, MAP kinase. Results : 1. Compared with normal cell, the inhibition of cell growth reduced in proportion with the dose of cobrotoxin(0-16nM) in PC-3. 2. Cell viabilities of 0.1, 1, 4nM cobrotoxin treatment were decreased and those of 8, 16nM were decreased significantly. 3. S phase of cell cycle was decreased at the group of 1, 2, 4, 8, 16nM cobrotoxin, but M phase was increased at 0.1, 1, 2, 4, 8, 16nM cobrotoxin. 4. Cox-2 expression after cobrotoxin was peaked at 12hours and was decreased significantly after 6, 12, 24 hours. 5. The expression of Cdk4 was decreased dose-dependently at 1, 2, 4, 8nM cobrotoxin and was decreased siginificantly at 4, 8nM Cyclin D1 was decreased at 1, 2, 4, 8nM and Cycline E was not changed. Cycline B was decreased at 1, 2, 4, 8nM dose-dependently and was decreased siginificanlty at 2, 4, 8nM. 6. The expression of Akt was decreased at 1, 2, 4, 8nM dose-dependently and was decreased significantly at 2, 4, 8nM. 7. ERK was increased at 1, 2nM and decreased at 4, 8nM, p-ERK was increased at 1, 2, 4 nM, but decreased at 8nM. JNK and p-JNK were increased at 1, 4, 8 nM. p38 was increased at 2nM p-p38 was increased at lnM but decreased significantly at 2, 4, 8nM. 8. The nucli of normal cells were stained round and homogenous in DAPI staining, but those of PC-3 were stained condense and splitted. Apoptosis was increased dose-dependently at 2, 4, 8, 16nM and increased significantly at 2, 4, 8, 16nM. 9. Bax wasn`t changed at 1, 2, 4, 8nM and Bcl-2 was decreased significantly at 1, 2, 4, 8nM. Caspase 3 and 9 weren`t changed at 1, 2, 4nM but were decreased significantly at 8nM. Conclusions : These results indicate that cobrotoxin inhibits the growth of prostate Cancer cells, has anti-cancer effects by inducing apoptosis.