• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.9 no.1
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• pp.1-15
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• 1996

The purpose of this research was to investigate effect of water extract of DangKwi-Eum-Ja ka Sumsoo(DESE) on the cytotoxicity of human epidemloid cell, A431 cells. The effects of DESE on the proliferation of A431 cells, Balb/c 3T3 cells, mouse thymocytes and splenocnes were estimated by MTT colorimetric assay, and nitric oxide production from mouse peritoneal macrophage was estimated by Griess method. DESE inhibited the proliferation of A431 cells at $10{\mu}g/ml$, and did not affect the proliferation of Balb/c 3T3 cells. DESE decreased the cytotoxicity of mitomycin C or cisplatin on A431 cells, increased the cytotoxicity of mitomycin C or cisplatin on Balb/c 3T3 cells. DESE inhibited the proliferation of mouse thymocytes and splenocytes at $100{\mu}g/ml$. DESE did not affect the nitric oxide production from mouse peritoneal macrophage in vitro, but decreased the nitric oxide production from DESE-treated mouse peritoneal macrophage.

• BMB Reports
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• v.34 no.3
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• pp.189-193
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• 2001

Curcumin a yellow pigment from Curcuma Tonga, has been known to possess antioxidative and anticarcinogenic properties, as well as to induce apoptosis in some cancer cells. There have been, however, several contradictory reports that hypothesized curcumin (a hydrophobic molecule) can bind a membrane Gpid bilayer and induce nonspecific cytotoxicity in some cell lines. Why curcumin shows these contradictory effects is unknown. In A-431 cells, growth inhibition by curcumin is due mostly to the specific inhibition of the intrinsic tyrosine kinase activity of the epidermal growth factor receptor, as reported earlier by Korutla et al. Thus, we assumed that the cell death of A-431 by curcumin might be due to the specific induction of apoptosis. In this paper we clearly show that curcumin induces apoptosis in A-431 cells. The cureumin-induced cell death of A-431 exhibited various apoptotic features, including DNA fragmentation and nuclear condensation. Furthermore, the curcumin-induced apoptosis of A-431 cells involved activation of caspase-3-like cysteine protease. Involvement of caspase-3 was further confirmed by using a caspase-3 specific inhibitor, DEVD-CHO. In another study, decreased nitric oxide (NO) production was also shown in A-431 cells treated with curcumin, which seems to be the result of the inhibition of the iNOS expression by curcumin, as in other cell lines. However, 24 h after treatment of curcumin there was increased NO production in A-431 cells. This observation has not yet been clearly explained. We assumed that the increased NO production may be related to denitrosylation of the enzyme catalytic site in caspase-3 when activated. Taken together, this study shows that the cell death of A-431 by curcumin is due to the induction of apoptosis, which involves caspase-3 activation.

• BMB Reports
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• v.31 no.3
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• pp.245-248
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• 1998

Human epidermoid carcinoma A431 cells have an extraordinarily large number of epidermal growth factor (EGF) receptors, and their growth is inhibited by EGF, which results in growth arrest at the Gl phase. In order to investigate the EGF-mediated inhibition mechanism, the expression level of DNA topoisomerase (topo) II was analyzed after EGF treatment. As a result, it was shown that EGF treatment lowered the amount of 170 kDa topo II (topo $II{\alpha}$) but not 180 kDa (topo $II{\beta}$). However, the A431 cell variant resistant to EGF was not sensitive to EGF treatment. These results suggest that EGF-induced growth arrest of A431 cells may be closely related to the depletion of topo $II{\alpha}$.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.7
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• pp.2813-2818
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• 2015

Objective: To investigate the regulatory effect of curcumin on expression of signal transducer and activator of transcription 3 (STAT3) in skin squamous cell carcinoma tissues as well as possible mechanisms of curcumin in prevention and treatment of skin squamous cell carcinoma. Materials and Methods: Highly invasive A431 cells were treated with curcumin at various doses .The cytotoxic effects of treatment with 5, 10, 15, 20, 25, 30, 35, 40 and 50 umol/L curcumin for 24, 48 and 72 hours on A431 cells were measured by MTT assay. The invasion capacity of cells treated with 5, 10 and 15 umol/L curcumin was measured by Transwell test, while adhesive ability was assessed by cell adhesion assay. The effects of 5,10 and 15 umol/L curcumin on expression levels of STAT3 were determined by Western blotting and on transcription levels of STAT3 mRNA by RT-PCR. Results: Treatment with curcumin at a doses of more than 15 umol/L for more than 24 hour inhibited the growth of A431 cells in a time-and dose-dependent fashion (p<0.001). The doses of 15 umol/L and less for 24 hours showed no significant cytotoxic effects on the cells, survival rates being more than 85%.The invasion and adhesive abilities decreased gradually with the increasing curcumin concentration, 15 umol/L exerting the strongest inhibitory effects (p<0.05). Curcumin showed significant dose-dependent inhibitory effects on the transcription level of STAT3 mRNA (p<0.05). Conclusions: Curcumin may reduce the invasive ability of A431 cells by inhibiting the activation of STAT3 signal pathway and expression of STAT3 as a target gene in the pathway.

• Microbiology and Biotechnology Letters
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• v.21 no.1
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• pp.47-53
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• 1993

Antibiotics KG-431A and KG-431B were isolated from the fermentation broth of the Clostridium sp. KH-431. As we have shown previously, only KG-431B was successful to recrystallize. These antibiotics showed antimicrobial activities against broad spectrum of bacteria and fungi. KG-431B also showed anticancer activity against some animal tumor cells according to the SRB method. Physico-chemical properties of KG-431B were determined using UV, IR, NMR and Mass spectra. It was identified to be 3-Indole propionic acid and the structure of the KG-431A is currently under investigation.

• Archives of Pharmacal Research
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• v.19 no.6
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• pp.490-496
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• 1996

Naphtodianthrone hypericin produced a potent antitumor activity in vitro against several tumor cells. However, it did not show any cytotoxicity on normal cells such as Macaccus rheus monkey kidney cells (MA-104) and primary cultured rat hepatocytes up to $500{\mu}M$ concentration. Hypericin added to A431 human epidermoid carcinoma cell membrane inhibited the autophosphorylation of the epidermal growth factor (EGF) receptor and the tyrosine phosphorylation of RR-SRC peptide catalyzed by an EGF-receptor. Similarly, treatment of the A431 cells with hypericin inhibited the tyrosine phosphorylation of EGF-dependent endogenous EGF-receptor by western blotting analysis. Hypericin also inhibited the T cell PTK, $P56^{lck}$, in a dose-dependent fashion with an $IC_{50}=5{\mu}M$. The tyrosine phosphorylation, on RR-SRC peptide and EGF-induced receptor autophosphorylation, either in vitro or in intact cells was inhibited by hypericin at the same concentration as that in A431 cell proliferation. These data suggest that hypericin directly inhibits EGF-receptor and $P56^{lck}$ PTK activity in vitro and can mediate such action in vivo.

• The Journal of Internal Korean Medicine
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• v.18 no.1
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• pp.231-241
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• 1997

The purpose of this research was to investigate effect of water extract of Euphorbiae Pekinensis Radix and Moutan Cortex Radicis on the proliferation of human cancer cell-lines. The effects of Euphorbiae Pekinensis Radix and Moutan Cortex Radicis on the proliferation of A431, HeLa, MOLT-4, K562 cells, Balb/c 3T3 cells, mouse thymocytes, splenocytes and human lymphocytes were estimated by MTT colorimetric assay. The results were as follows; 1. In proliferation of A431, HeLa, MOLT-4 and K562 cell-lines, Euphorbiae Pekinensis Radix and Moutan Cortex Radicis inhibited the proliferation of K562 cells. 2. In the combined effect of Euphorbiae Pekinensis Radix and mitomycin C, Moutan Cortex Radicis and mitomycin C, all herbs stimulated the proliferation of MOL T-4 cells. 3. Euphorbiae Pekinensis Radix and Moutan Cortex Radicis did not inhibited the proliferation of Balb/c 3T3 cells. 4. Euphorbiae Pekinensis Radix and Moutan Cortex Radicis stimulated the proliferation of mouse thymocytes. 5. Euphorbiae Pekinensis Radix and Moutan Cortex Radicis stimulated the proliferation of mouse splenocytes. 6. Euphorbiae Pekinensis Radix and Moutan Cortex Radicis stimulated the proliferation of human lymphocytes.

• The Journal of Korean Medicine
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• v.17 no.2 s.32
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• pp.303-310
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• 1996

The purpose of this study was to investigate effect of water extract of Carthami Flos on the proliferation of human cancer cell-lines. The effects of Carthami Flos on the proliferation of A431, HeLa, MOLT-4, K562 cells, Balb／c 3T3 cells, mouse thymocytes, splenocytes and human lymphocytes were estimated by MTT colorimetric assay. The results were as follows; 1. Carthami Flos did not effect A431, HeLa, MOLT-4, K562 cells. 2. The cytotoxicity of mitomycin C on K562 cells was increased by the combination of Carthami Flos. 3. Carthami Flos inhibited the proliferation of Balb／c 3T3 cells. 4. Carthami Flos stimulated the proliferation of thymocytes. 5. Carthami Flos stimulated the proliferation of splenocytes. 6. Carthami Flos stimulated the proliferation of human lymphocytes.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.12 no.1
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• pp.79-98
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• 1999

The purpose of this Study was to investigate effect of TakliSodokSan(TSS) on the anti-tumor, immunocytes and nitric oxide(NO) production from mice peritoneal macrophages. This Study estimated the proliferation of L1210 cell lines, A431 cell lines, Hep-G2 cell lines, K562 cell lines, 3T3 cell lines, mouse thymocytes and mouse splenocytes and NO production from pcritoneal macrophages in vitro, and estimated the proliferation of L1210 cells, thymocytes and splenocytcs, NO production from peritoneal macrophages and body weight in L1210 cells-transplanted mice in vivo. The results were obtained as follows; 1. TSS inhibited significantly the proliferation of L1210, A431, Hep-G2, K562 cell lines in vitro. 2. TSS accelerated the proliferation of mice thymocytes and splenocytes in vitro. 3. TSS was not increased the nitric oxide production from mice peritoneal macrophages in vitro. 4. TSS inhibited significantly the proliferation of L1210 cells in Ll210 cells∼transplanted mice. 5. TSS accelerated the proliferation of mice thymocytes and splenocytes In L1210 cells-transplanted mice. 6. TSS was increased significantly the nitric oxide production from mice peritoneal macrophages in L1210 cells-transplanted mice. 7. TSS was increased the body weight as comparing with control group in Ll210 cells-transplanted mice.

• Journal of Korean Academy of Oral and Maxillofacial Radiology
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• v.29 no.1
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• pp.327-339
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• 1999

Objectives: The purpose of this study was to aid in the prediction of tumor cell tolerance to radiotherapy and/or chemotherapy. Material and Methods: Human epidermoid carcinoma A-431 cell lines were irradiated by 2, 4, 6, 8, 10Gy at a dose rate of 210cGy/min using /sup 60/Co Irradiator ALDORADO 8 and then were exposed to bleomycin or cisplatin at concentration of 2㎍/㎖ for 1 hour. The viable cells were determined for each radiation dose and/or each drug at the 4th day and cell surviving curves were obtained using semiautomated MTT assay. Results: The surviving fraction after irradiation of 2Gy was 0.99, and there was not significant difference of surviving fraction in comparison with the control group on A-431 cell line(P>0.05). But there were significant differences of surviving fractions at doses of 4, 6, 8, 10Gy in comparison with the control group(P<0.05). The cytotoxicity of bleomycin or cisplatin was significantly different in comparison with the control group on A-43l cell line (P<0.05). And the cytotoxicity of cisplatin was greater than that of bleomycin on A-431 cell line (P<0.05). There were significant differences of surviving fractions after irradiation of 2, 4, 6, 8, 10Gy with bleomycin or cisplatin in comparison with each group of irradiation only on A-431 cellline(P<0.05). There were significant differences of surviving fractions between the groups of irradiation with bleomycin and cisplatin at doses of 2, 4Gy(P<0.05), but there were not significant differences of surviving fractions at doses of 6, 8, 10Gy on A-431 cell line (P>0.05).