• Korean Journal of Oriental Medicine
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• v.18 no.1
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• pp.75-84
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• 2012

Objective : The purpose of this study was to investigate the anti-cancer effects of Sophorae Radix and the effects of Doxorubicin (DOX) in human breast adenocarcinoma cells (MCF-7). Method : We used human breast adenocarcinoma cell line, MCF-7 cells. We examined cell death by MTT assay and caspase 3 assay with Sophorae Radix. To examine the inhibitory effects of Sophorae Radix, cell cycle analysis was done the MCF-7 cells after three days with Sophorae Radix. The reversibility of Sophorae Radix was examined on one day to five days treatment with 100 ${\mu}g/ml$ Sophorae Radix. Result : Sophorae Radix inhibited the growth of MCF-7 cells in a dose-dependent fashion. Also we showed that Sophorae Radix induced apoptosis in MCF-7 cells by MTT assay, caspase 3 assay and sub-G1 analysis. Sophorae Radix combined with DOX markedly inhibited the growth of MCF-7 cells compared to Sophorae Radix or DOX alone. After 3 days treatment of MCF-7 cells with Sophorae Radix, the fraction of cells in sub-G1 phase was much higher than that of the control group. Conclusion : Our findings provide insight into unraveling the effects of Sophorae Radix in human breast adenocarcinoma cells and developing therapeutic agents against breast cancer.

• Journal of Physiology & Pathology in Korean Medicine
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• v.25 no.5
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• pp.857-862
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• 2011

The purpose of this study is to investigate the anti-proliferative mechanism by Trichosanthes kirilowii (TCK) in MCF-7 human breast carcinoma cell. In this study, we used human breast cancer cell line, Michigan cancer foundation-7 cells (MCF-7 cells). They were co-incubated with 30~200 ${\mu}g$/ml TCK for 48 hours, and cell viability was measured by Water-soluble tetrazolium salt-1 (WST-1) assay. After MCF-7 cells were exposed to 60 ${\mu}g$/ml of TCK for 0, 3, 6, 12, 24, 48 hours, We performed flow analysis cytometry sorting(FACS) and western blot analysis. We investigated the effect of dose-dependent cell growth inhibition by TCK, which could be proved by WST-1 assay. Also, flow cytometry analysis showed that TCK increased percentage of subG1 phase and G2/M phase cell cycle. In addition, TCK induced apoptosis through the expression of caspase-9, -3 and poly(ADP-ribose) polymerase(PARP) activation. Moreover, we showed that ATM-dependent G2/M phase arrest by DNA damage and phosphorylation of chk2, cdc25C, cdc2(Tyr15). Taken together, these results suggest that by G2/M phase arrest through DNA damage and inducing of apoptosis through intrinsic pathway, TCK may have potential tumor suppressor in breast cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.18
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• pp.8113-8117
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• 2016

Glehnia littoralis (GL) is widely used as an oriental medicine for cough, fever, stroke and other disease conditions. However, the anti-cancer properties of GL on MCF-7 human breast cancer cells have not been investigated. In order to elucidate anti-cancer properties and underlying cell death mechanisms, MCF-7cells ($5{\times}10^4/well$) were treated with Glehnia littoralis root extract at 0-400 ug/ml. A hot water extract of GL root inhibited the proliferation of MCF-7 cells in a dose-dependent manner. Analysis of the cell cycle after treatment of MCF-7 cells with increasing concentrations of GL root extract for 24 hours showed significant cell cycle arrest in the G1 phase. RT-PCR and Western blot analysis both revealed that GL root extract significantly increased the expression of p21 and p27 with an accompanying decrease in both CDK4 and cyclin D1. Our reuslts indicated that GL root extract arrested the proliferation of MCF-7 cells in G1 phase through inhibition of CDK4 and cyclin D1 via increased induction of p21 and p27. In summary, the current study showed that GL could serve as a potential source of chemotherapeutic or chemopreventative agents against human breast cancer.

• Korean Journal of Plant Resources
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• v.25 no.5
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• pp.647-651
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• 2012

The objective of this study was to investigate the anticancer effects of the extracts of oriental melon seeds. Various solvent extracts of oriental melon seeds were prepared and their anticancer effects were examined using in vitro MTT and CV assays. The anticancer effects of various extracts of oriental melon seeds were also examined in five human cancer cell lines including A549, AGS, HT-29, MCF-7 and HepG2. The ethanol extract of heated oriental melon seeds showed the potent cytotoxic effects especially against mouse hepatoma cell line(Hepa1c1c7), human hepatoma cell line(HepG2) and human breast cancer cell line(MCF-7). These data suggest that oriental melon seeds can be a promising anticancer agent against human liver and breast cancer.

• Journal of Food Hygiene and Safety
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• v.22 no.3
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• pp.209-212
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• 2007

To evaluate the estrogenic activities of di-ethyl hexyl phthalate (DEHP) and di-butyl phthalate (DBP), two phthalates known as endocrine disrupters, we used MCF-7 human breast cancer cell line. As results, DBP and DEHP had estrogenic effects. In brief, the concentration of maximal MCF-7 cell proliferation was $10^{-7}M\;and\;10^{-8}M$ for DEHP and DBP, respectively. The ratio of maximal cell yield of the test compounds to that of $17{\beta}-estradiol$ was 87.5% for DEHP and 73.4% for DBP. In summary, both DEHP and DBP had cell proliferation potencies in the MCF-7 cell. Potencies ranged from approximately 10 to 100 times less than 17beta-estradiol. DBP was stronger than DEHP in the concentration of maximal efficacy. However, DEHP was stronger than DBP in the MCF-7 cell proliferation. Results from this study suggested that DEHP and DBP may play an important role in the estrogenic activity. Therefore, it is suggested that DEHP and DBP are estrogenic.

• The Journal of Internal Korean Medicine
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• v.43 no.4
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• pp.529-541
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• 2022

Objectives: Acanthopanax senticosus is a tree used in traditional medicine for various diseases. In this study, we investigated the anti-cancer effects of a water extract of Acanthopanax senticocus fruit (ASF) on 2 human breast cancer cell lines (MCF-7 and MDA-MB-231). Methods: The MTT assay was used to assess cell proliferation. The expression of apoptosis-related genes was assessed by quantitative real-time PCR. Results: ASF treatment caused a dose-dependent inhibition of cell growth in both estrogen-independent MDA-MB-231 and estrogen-dependent MCF-7 breast cancer cells. ASF decreased mRNA expression of the apoptotic suppressor gene Bcl-xL, and increased mRNA expression of proapoptotic genes. ASF increased the mRNA expression of p21 and RIP-1 in both cell types. ASF decreased the mRNA expression of survivin in the MCF-7 cell line. Conclusions: ASF exhibits anti-cancer activity involving apoptotic cell death.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.6
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• pp.2979-2984
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• 2012

Recent studies have indicated a link between levels of cyclooxygenase-2 (COX-2) and development of the multidrug resistance (MDR) phenotype. The ATP-binding cassette sub-family G member 2 (ABCG2) is a major MDR-related transporter protein that is frequently overexpressed in cancer patients. In this study, we aimed to evaluate any positive correlation between COX-2 and ABCG2 gene expression using the COX-2 inducer 12-O-tetradecanoylphorbol-13-acetate (TPA) in human breast cancer cell lines. ABCG2 mRNA and protein expression was studied using real-time RT-PCR and flow cytometry, respectively. A significant increase of COX-2 mRNA expression (up to 11-fold by 4 h) was induced by TPA in MDA-MB-231 cells, this induction effect being lower in MCF-7 cells. TPA caused a considerable increase up to 9-fold in ABCG2 mRNA expression in parental MCF-7 cells, while it caused a small enhancement in ABCG2 expression up to 67 % by 4 h followed by a time-dependent decrease in ABCG2 mRNA expression in MDA-MB-231 cells. TPA treatment resulted in a slight increase of ABCG2 protein expression in MCF-7 cells, while a time-dependent decrease in ABCG2 protein expression was occurred in MDA-MB-231 cells. In conclusion, based on the observed effects of TPA in MDA-Mb-231 cells, it is proposed that TPA up-regulates ABCG2 expression in the drug sensitive MCF-7 breast cancer cell line through COX-2 unrelated pathways.

• The Journal of Korean Obstetrics and Gynecology
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• v.21 no.3
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• pp.18-33
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• 2008

Purpose: The research is to investigate the effect of TFE on apoptosis of human-derived breast cancer cells, to find out the relationship with apoptosis. Methods: Human-derived breast adenocarcinoma cell line, MCF-7 cells were treated by TFE with various concentration. The inducement effect of TFE on cell apoptosis was observed with MTT assay and the relationship between the treatment and apoptosis was investigated with FACS analysis, TUNEL assay and DNA laddering assay and the change in the protein levels of PARP and caspase-3 activities were also observed. The release of cytochrome-c was observed to find out the pathway of apoptosis induced by TFE. Results: The cell apoptosis was significantly induced in MCF-7 cells treated with TFE in concentration-dependent and time-dependent manner. It was verified by FACS analysis, TUNEL assay, DNA laddering assay that cell-death was caused not by necrosis but by apoptosis. The activity of PARP and caspase were increased concentration-dependently. The release of cytocrome-c was decreased in proportion to the concentration of the fruit extract. It therefore demonstrated that mitochondria were involved in apoptosis induced by TFE. The appearance of Bcl-2 protein was decreased concentration-dependently. Conclusion: The treatment by TFE induced apoptosis of human breast adenocarcinoma cell line, MCF-7. It seems likely that cell-death was caused by apoptosis and mitochondria were involved in it. The mechanism of protein change causing apoptosis seems related to the inhibition of Bcl-2 protein, the promotion of inversion from cytochrome-c into cytosol, the activation of caspase and the promotion of PARP cleavage.

• Molecular & Cellular Toxicology
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• v.2 no.1
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• pp.15-20
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• 2006

Genistein is a potent, plant-derived isoflavone that displays estrogenic activity at low concentrations but inhibits proliferation at high amounts. However, the molecular mechanism of genistein is not completely understood. In the present study, the biphasic effects (estrogenic and antiestrogenic activity) of genistein on the growth of MCF-7 cells were identified. Genistein within a low range of concentration, $1-10\;{\mu}M$, stimulated proliferation, while $50-100\;{\mu}M$ caused apoptotic cell death. Additionally, genistein at a low concentration induced estrogen receptor (ER)-mediated gene expression and ER phosphorylation. When pre-treated with PD98059, an MEK inhibitor, ER-mediated gene expression and ER phosphorylation by genistein were noticeably increased. However, the increased gene expression and phosphorylation did not enhance cell proliferation. Moreover, it was observed that ER-mediated signaling performs an important role in the MAPK pathway. The proliferation and apoptosis in genistein-treated MCF-7 cells were partially dependent on the Bcl-2 level. The addition of IC1 182, 780, an estrogen receptor antagonist, inhibited Bcl-2 expression induced by genistein. This study suggests that there is a close relationship between Bcl-2 and the ER signaling pathways in MCF-7 cells.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.sup3
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• pp.293-297
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• 2016

TRAIL, tumor necrosis factor (TNF)-related apoptosis-inducing ligand belongs to one of important cytokine superfamilIES, tumor necrosis factor ($TNF{\alpha}$). TRAIL-2 receptor agonists activate several cell signaling pathways in cells in different manners and could lead to apoptosis or necrosis. Agonistic egg yolk antibodies like IgY which have been developed in a selective manner could activate TRAIL death receptors such as TRAIL-2 (DR5) and thus apoptosis signaling. We here investigated induction of apoptosis in human breast cancer cells (MCF7 cell line) by an IgY produced against an 21 aminoacid epitope of the human TRAIL-2 receptor. As the first step a small peptide of 21 aminoacids choosen from the extracellular domain of DR5 protein was produced with a peptide synthesizer. After control assays and confirmation of the correct amino acid sequence, it was injected to hens immunized to achieve high affinity IgYs. At the next step, the produced IgYs were extracted and examined for specificity against DR5 protein by ELISA assay. Subsequently, the anticancer effect of such IgYs was determined by MTT assay in the MCF7 human breast cancer cell line. The produced peptides successfully immunized hens and the produced antibodies which accumulated in egg yolk specifically recognized the DR5 protein. IgYs exerted significant toxicity and killed MCF7 cells as shown by MTT assay.