• Proceedings of the Korean Society of Applied Pharmacology
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• 1997.04a
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• pp.107-107
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• 1997

Cytochrome P450 enzymes have been intensively investigated in hepatic tissues and several mammalian cell lines. Compared to most studies about cytochrome P450 isozymes in liver in vivo and hepatic, cell lines in vitro, the study of cytochrome P450IA1 in human breast cancer cells could be very important to understand the mechanism of the regulation of CYPIA1 gene expression and cell growth. MCF-7 human breast cancer cells are well characterized to study estrogen and antiestrogen action due to the fact that they contain high level of estrogen receptor and have biological markers characterized. And also MCF-7 cells express high level of arylhydrocarbon hydroxylase activity and human cytochrome P450IA1 cDNA was cloned from MCF-7 cells. Ah receptor was characterized in many breast cancer cell lines and polycyclic aromatic hydrocarbon such as 3-MC induced the expression of CYPIA1 gene and cytochrome P450- dependent monooxygenase activity. We undertook a study to examine the effect of estrogens and other chemicals on the regulation of human CYPIA1 gene expression in MCF-7 cells via RTPCR analysis, that might help us to understand the mechanism of the regulation of CYPIA1 gene expression and MCF-7 cell growth. Expression vector containing the functional 5'-regulatory region of human CYPIA1 fused to the CAT reporter gene was transfected into estrogen receptor positive MCF-T cells or estrogen receptor negative MDA-MB-231 cells. After these cells were treated with various chemicals, RTPCR was carried out to measure both CYPIA1 mRNA and CAT mRNA levels. 1nM 3-MC increased in both P450 and CAT mRNA levels over those of control by two folds in MCF-7 cells but does not in MDA-MB-231 cells. Estrogen or tamoxifen or retinoic acid or chrysin decreased in both P450 and CAT mRNA levels that were induced by 3-MC in MCF-7 when each chemical was administered with 3-MC concomitantly. These results suggested that the level of CYPIA1 gene expression is modulated with estrogen-related molecules and make it possible to speculate that ER is related to CYPIA1 gene expression and cell growth in breast cancer cells. [Supported by grants from the Korean Ministry of Education ]

• The Journal of Korean Obstetrics and Gynecology
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• v.20 no.3
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• pp.35-44
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• 2007

Purpose: This study was conducted to investigate the anti-proliferative effects of Ulmi Pumilae Cortex Extracts(UPCE) on MCF-7(human, breast, adenocaecinoma) and NIH3T3 (human, murine, fibroblast). Methods: MCF-7 cells and NIH3T3 cells were cultured and seeded in cell culture plates, respectively. UPC was extracted with hot water and then further fractionated it into five types: hexane, chloroform, ethyl acetate, butanol, and water soluable fractions. These five different fractions from UPCE were tested for their anti-proliferative effects on MCF-7 cells and NIH3T3 cells by MMT assay. Results: Among the five solvent-fractions of UPCE, n-hexane fraction and ethyl acetate fraction showed a strong anti-proliferative effects on MCF-7 cells but they displayed significant cytotoxicity on NIH3T3 cells, too. On the other hand, chloroform fraction showed a marked anti-proliferative effects on MCF-7 cells and low cytotoxicity on NIH3T3 cells. Conclusion: Chloloform fraction from UPCE showed selective anti-cancer activities on human breast cancer cell MCF-7 relatively to the other fractions.

• Journal of Ginseng Research
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• v.37 no.2
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• pp.201-209
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• 2013

Ginsenoside, one of the active ingredients of Panax ginseng, has a variety of physiologic and pharmacologic effects. The purpose of this study was to explore the effects of ginsenoside Rd (G-Rd) on melastatin type transient receptor potential 7 (TRPM7) channels with respect to the proliferation and survival of AGS and MCF-7 cells (a gastric and a breast cancer cell line, respectively). AGS and MCF-7 cells were treated with different concentrations of G-Rd, and caspase-3 activities, mitochondrial depolarizations, and sub-G1 fractions were analyzed to determine if cell death occurred by apoptosis. In addition, human embryonic kidney (HEK) 293 cells overexpressing TRPM7 channels were used to confirm the role of TRPM7 channels. G-Rd inhibited the proliferation and survival of AGS and MCF-7 cells and enhanced caspase-3 activity, mitochondrial depolarization, and sub-G1 populations. In addition, G-Rd inhibited TRPM7-like currents in AGS and MCF-7 cells and in TRPM7 channel overexpressing HEK 293 cells, as determined by whole cell voltage-clamp recordings. Furthermore, TRPM7 overexpression in HEK 293 cells promoted G-Rd induced cell death. These findings suggest that G-Rd inhibits the proliferation and survival of gastric and breast cancer cells by inhibiting TRPM7 channel activity.

• Bulletin of the Korean Chemical Society
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• v.34 no.11
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• pp.3317-3321
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• 2013

A series of new 3-alkylamino-6-allylthio-pyridazine derivatives was synthesized through allythiolation and amino-de-halogenation and were expected to have anti-proliferative activity. 6-Allylthio-3-chloropyridazine was prepared from the reaction of 3,6-dichloropyridazine with allylmercaptan and sodium hydroxide. The alkylamines such as methylamine and the dialkylamines such as dimethylamine were introduced into the 3-position of the pyridazine ring. These new compounds showed anti-proliferative activities against MCF-7 human breast cancer cells in CCK-8 assays. These compounds are thus promising candidates for chemotherapy of breast cancer. Two compounds, 14 and 15, showed higher potencies for inhibiting growth of breast cancer cells than did 5FU. This suggests the potential anti-proliferative activity of these compounds.

• Environmental Mutagens and Carcinogens
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• v.23 no.2
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• pp.45-50
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• 2003

Biological activities of PAHs are not known although PAHs are considered as carcinogens. Recent industrial society has human widely exposed to PAHs (polynuclear aromatic hydrocarbons) that are comming from the incomplete combustion of organic material as wider spread environmental contaminants. Our laboratory have been studied the effect of PAHs in the human breast cancer MCF-7 cells. In this study, we examined the human breast cancer MCF-7 cells as a new system to evaluate bioactivity of PAHs. We have selected 13 PAHs to examine bioassay using CYP1A1-luciferase reporter gene expression system where CYP1A1 1.6 Kb 5flanking region DNA was cloned in front of luciferase reporter gene and this plasmid was transfected into MCF-7 cells transiently. This cells then used for the study to observe the effect of PAHs. We demonstrated that PAHs induced the CYP1A1 promoter, CYP1A1 mRNA and 7-ethoxyresolufin O-deethylase (EROD) activities in a concentration-dependant manner. None of PAHs that we have tested showed stronger stimulatory effect on CYP1 gene expression than TCDD. Benz(a)anthracene and benzo(b)fluoranthene were weak responders to CYP1A1 promoter activity stimulation, CYP1A1 mRNA and EROD induction in MCF-7 cells and these chemicals seemed to respond less either CYP1A1 mRNA or EROD than CYP1A1 promoter activity. Benzo(k)fluoranthene, chrysene, and dibenzo(a, h)anthracene showed strong response to CYP1A1 promoter activity stimulation, CYP1A1 mRNA increase and also EROD induction in MCF-7 cells. Results of dose response study suggested that two strong responding PAHs, such as benzo(k)fluoranthene and dibenzo(a, h)anthracene might be mediated through Aryl hydrocarbon receptors system in MCF-7 cells.

• Journal of Physiology & Pathology in Korean Medicine
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• v.24 no.3
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• pp.385-389
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• 2010

Butein(3,4,2',4-tetrahydroxychalcone) has been reported anticancer effects in several cancer type, which is prostate, bladder cancer but breast cancer is not. This study was to investigate the antiproliferative effects by butein(3,4,2',4-tetrahydroxychalcone) in MCF-7 human breast carcinoma cells. We invastigated the effects of dose-dependently cell growth inhibition by butein, which could be proved by WST-1 assay. Also, flow cytometry analysis was butein increase percentage of subG1 phase. As well as, butein induces apoptosis through the expression of caspase-8,-3 and poly(ADP-ribose) polymerase(PARP) activation but not in DMSO treated cells. Taken together, this results suggest that butein induced MCF-7 apoptosis through extrinsic pathway and thus may have potential tumor suppressor in breast cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.4
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• pp.1617-1620
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• 2012

Background: Gold nanoparticles have recently been investigated with respect to biocompatibility according to their interactions with cells. The purpose of this study was to examine cytotoxicity and apoptosis induction by well-characterized gold nanoparticles in human breast epithelial MCF-7 cells. Methods: Apoptosis was assessed by TUNEL, cytotoxicity by MTT assay and caspase 3, 9, p53, Bax and Bcl expression by real-time PCR assays. Results: Gold nanoparticles at up to $200\;{\mu}g/mL$ for 24 hours exerted concentration-dependent cytotoxicity and significant upregulation of mRNA expression of p53, bax, caspase-3 & caspase-9, whereas expression of antiapoptotic bcl-2 was down-regulated. Conclusion: To the best of our knowledge this is the first report showing that gold nanoparticles induce apoptosis in MCF-7cells via p53, bax/bcl-2 and caspase pathways.

• Journal of Food Hygiene and Safety
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• v.25 no.3
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• pp.209-214
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• 2010

Metastasis is the primary cause of from breast cancer mortality. Cell migration and invasion play important roles in neoplastic metastasis. Matrix metalloproteinase-9 (MMP-9), which degrades the extracellular matrix (ECM), plays an important role in cancer cell invasion. NF-${\kappa}B$ is transcription factor important in the regulation of MMP-9, as the promoter of MMP-9 gene contains binding sites for NF-${\kappa}B$. Brazilin, an active component of sappan wood (Caesalpinia sappan), decreases TPA-induced MMP-9 expression and invasion in MCF-7 cells. Also, brazilin suppressed NF-${\kappa}B$ activation in TPA-treated MCF-7 cells. Taken together, we demonstrated that the inhibition of TPA-induced MMP-9 expression and cell invasion by brazilin is mediated by the suppression of the NF-${\kappa}B$ pathway in MCF-7 cells. This result suggest brazilin provide a potential therapeutic app roach for the treatment of breast cancer.

• BMB Reports
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• v.39 no.4
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• pp.448-451
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• 2006

Chemopreventive and cytotoxic effect of genistein against human breast cancer cell lines was investigated. Genistein inhibited cell proliferation in estrogen receptor-positive (MCF-7) and estrogen receptor-negative (MDA-MB-231) human breast carcinoma cell lines. Cytochrome P450 (CYP) 1A1-mediated ethoxyresorufin O-deethylase (EROD) activity was inhibited by genistein in a concentrationdependent manner. Genistein significantly inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced cyclooxy-genase-2 activity and protein expression at the concentrations of 10 (p < 0.05), 25 (p < 0.05) and 50 mM (p < 0.01). In addition, ornithine decarboxylase (ODC) activity was reduced to 53.8 % of the control after 6 h treatment with 50 mM genistein in MCF-7 breast cancer cells. These results suggest that genistein could be of therapeutic value in preventing human breast cancer.

• International Journal of Industrial Entomology and Biomaterials
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• v.27 no.2
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• pp.228-236
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• 2013

Breast cancer is one of the most common cancers among women worldwide. Recently anticancer agents have been developed using natural substances. To evaluate the anticancer effect of hydrolysates of silk fibroin (HSF), we investigated the effect of HSF on cell viability and apoptosis of a breast cancer cell line, MCF-7, induced through the mitochondrial pathway. The result showed that HSF decreased cell viability in MCF-7 cells in a dose- and time-dependent manner, resulting in an increase in the sub-G1 phase cell population. HSF increased the level of the pro-apoptotic Bax protein and decreased the levels of the anti-apoptotic Bcl-2 protein. In addition, HSF induced apoptosis in MCF-7 cells through a mitochondria-dependent pathway by increasing levels of cytochtome c, and cleavage of PARP. Taken together, these findings suggest that HSF inhibits the proliferation of MCF-7 breast cancer cells through a mitochondria and caspase dependent apoptotic pathway.