• 대한본초학회지
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• 제21권1호
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• pp.71-77
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• 2006

Objectives : This investigation was undertaken to evaluate the anti-proliferation of CURCUMAE LONGAE Rhizoma extracts using MCF-7, human breast cancer cells. Methods : MCF-7 cells were cultured in Dulbecco's modified Eagle's medium/F12 supplemented with 10% fetal bovine serum and antibiotics. At varying times after extract treatment, cells were harvested with scraper and processed for analysis of proliferation, cytotoxicity. Results : The extract of CURCUMAE LONGAE Rhizoma strongly inhibits the proliferation of MCF-7 cells in a dose and time-dependent manner. Sulforhodamine B assay showed that the addition of ethanol extract of CURCUlVIAE LONGAE Rhizoma reduced the viability of MCF-7 cells in a dose-dependent manner. Conclusion : So, it can be concluded that CURCUMAE LONGAE Rhizoma have an inhibitive effect on MCF-7 human breast cancer cells.

• Environmental Analysis Health and Toxicology
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• 제27권
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• pp.10.1-10.7
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• 2012

Objectives: In recent years, a number of structurally diverse Histone deacetylase (HDAC) inhibitors have been identified and these HDAC inhibitors induce growth arrest, differentiation and/or apoptosis of cancer cells in vitro and in vivo. This study aimed at investigating the antitumor activity of newly synthesized HDAC inhibitor, 3-(4-dimethylamino phenyl)-N-hydroxy-2-propenamide (IN-2001) using human breast cancer cells. Methods: We have synthesized a new HDAC inhibitor, IN-2001, and cell proliferation inhibition assay with this chemical in estrogen receptor-positive human breast cancer MCF-7 cells. Cell cycle analysis on MCF-7 cells treated with IN-2001 was carried out by flow cytometry and gene expression was measured by RT-PCR. Results: In MCF-7 cells IN-2001 showed remarkable anti-proliferative effects in a dose- and time-dependent manner. In MCF-7 cells, IN-2001 showed a more potent growth inhibitory effect than that of suberoylanilide hydroxamic acid. These growth inhibitory effects were related to the cell cycle arrest and induction of apoptosis. IN-2001 showed accumulation of cells at $G_2$/M phase and of the sub-$G_1$ population in a time-dependent manner, representing apoptotic cells. IN-2001-mediated cell cycle arrest was associated with HDAC inhibitor-mediated induction of CDK inhibitor expression. In MCF-7 cells, IN-2001 significantly increased $p21^{WAF1}$ expression. Conclusions: In summary, cyclin-dependent kinase (CDK) induced growth inhibition, possibly through modulation of cell cycle and apoptosis regulatory proteins, such as CDK inhibitors, and cyclins. Taken together, these results provide an insight into the utility of HDAC inhibitors as a novel chemotherapeutic regime for hormone-sensitive and insensitive breast cancer.

• 한국환경성돌연변이발암원학회지
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• 제24권2호
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• pp.51-66
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• 2004

Retinoids, better known as vitamin A, have been reported to inhibit the growth of several breast cancer cell lines in culture and to reduce breast tumor growth in animal models. Furthermore, retinoids can augment the action of other breast cancer cell growth inhibitors both in vitro and in vivo. Clinically, interest has increased in the potential use of retinoids for the prevention and treatment of human breast cancer. We have examine the effect of all-trans retinoic acid(tRA) and 9-cis retinoic acid(9-cis RA) on human breast cancer cell(MCF-10A, T47-D, MCF-7) proliferation using MTT assay and cell cycle analysis(FACS). Overexpression of cyclin D1 protein is observed in the majority of breast cancers, suggesting that dysregulated expression of cyclin D1 might be a critical event in breast cancer carcinogenesis. We investigated whether tRA and 9-cis RA might affect expression of cyclin D1 on human breast cancer cells(MCF-10A, T47-D, MCF-7) using RT-PCR and west-ern bolt. In MCF-10A cells, either tRA or 9-cis RA treatment did not affect the cell proliferation. In T47-D cells and MCF-7 cells, either tRA or 9-cis RA treatment showed the inhibition of the cell proliferation over control cells and also inhibit the estrogen stimulated cell proliferation when it was given together with estrogen. The effect of retinoids was dose- and time- dependent. T47-D cells treated with 1.0 $\muM$ tRA undergo G0/G1-phase arrest by Day 5. MCF-7 cells treated with 1.0 $\muM$ tRA undergo S-phase arrest by Day 5. All-trans retinoic acid(tRA) and 9-cis retinoic acid(9-cis RA) inhibited the cyelin D1 mRNA and protein expression levels of human MCF-7 and T47-D breast carcinoma cells in vitro. The data indicate that retinoids can reduce cyclin D1 expression levels in a variety of breast cell lines in vitro and result in inhibition of cell proliferation. tRA-mediated growth inhibition and cyclin D1 expression inhibition is more potent than 9-cis RA mediated that. tRA-mediated inhibition effect is more potent on T47-D cells than on MCF-7 cells. Our data suggest that retinoids activity is different according to property of cell lines. Future chemoprevention of breast cancer studies using retinoids will be necessary to determine the mechanism of the retinoids-mediated growth inhibition.

• Biomolecules & Therapeutics
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• 제17권3호
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• pp.288-292
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• 2009

Interactions between tumor cells and the extracellular matrix (ECM) strongly influence tumor development, affecting cell survival, proliferation and migration. Fibronectin, a major component of ECM, has been shown to interact with integrins especially the ${\alpha}5{\beta}1$ integrin. Cell invasion and metastasis are often associated with matrix metalloproteinases (MMPs) which are capable of digesting the different components of the ECM and basement membrane. MMP-2 is produced as a latent pro-MMP-2 (72 kDa) to be activated, resulting the 62 kDa active MMP-2. In this study, we investigated the effect of fibronectin on activation of pro-MMP-2 and the cellular invasiveness in H-Ras-transformed MCF10A human breast epithelial cells. Here we show that fibronectin induces activation of pro-MMP-2 and up-regulation of MT1-MMP and TIMP-2 in H-Ras MCF10A cells. These results demonstrate that H-Ras MCF10A cells secrete high levels of active MMP-2 when cultured with fibronectin, suggesting a possible interaction between the ECM network and H-Ras MCF10A cells to generate active MMP-2 which is important for proteolysis and ECM remodeling. Invasive and migratory abilities of H-Ras MCF10A cells were enhanced by fibronectin. Fibronectin up-regulated the expression of ${\beta}1$ integrin which may play a role in cellular responses exerted by fibronectin. Since acquisition of pro-MMP-2 activation can be associated with increased malignant progression, this study provides a mechanism for the cell surface-matrix degrading effect of fibronectin which will be crucial to breast cell invasion and migration.

• KSBB Journal
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• 제18권5호
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• pp.424-428
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• 2003

내분비계장애물질인 bisphenol A, nonylphenol, pentachlorophenol을 대상으로 여성 유방암세포 유래 MCF-7 세포주와 남성 전립선암세포 유래 PC-3 세포주에서 세포 증식효과를 MTT 방법으로 조사하였다. MCF-7 세포주에 이들 세 종류의 내분비계장애물질을 농도별로 처리하여 세포증식에 미치는 영향을 조사한 결과 모두 세포증식을 촉진하는 결과를 보였다. $10^{-7}$ M에서 $10^{-6}$ M 농도 범위에서 MCF-7 세포의 최대증식효과를 유도하였다. 그러나 PC-3 세포주의 경우에는 세포증식에 bisphenol A, nonylphenol, pentachlorophenol 모두 영향을 미치지 못하였다. 이러한 결과는 이들 세 종류의 내분비계 장애물질이 남성 전립선세포 유래인 PC-3 세포주의 증식에는 관여하지 않고 여성 유방암 세포에서 유래하고 에스트로젠 반응성인 MCF-7 세포주에만 증식효과를 갖는 사실을 보여주고 있으며 이는 bisphenol A, nonylphenol, pentachlorophenol이 여성호르몬인 에스트로젠과 유사한 역할을 한다는 사실을 보여주는 것이라 할 수 있다.

• 대한한의학방제학회지
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• 제24권4호
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• pp.283-288
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• 2016

Objectives : The purpose of this study was to investigate the anti-cancer effects of extract of Rhus verniciflua Stokes (RVS) in human breast cancer cell lines. Methods : In cultured human breast cancer MCF-7 cells, we investigated growth inhibitory effect of RVS. MCF-7 cells were cultured with various concentrations (0, 200, 300, and 400 ug/ml) of RVS at $37^{\circ}C$ for 24 h. We performed CCK-8 assay and flow cytometry for detection of Annexin V-PI staining. Results : As a result, RVS inhibits the cell growth and induction of apoptosis in dose dependent manner in MCF-7 breast cancer cells. Conclusion : RVS has anti-cancer activities and induced apoptosis in human breast cancer MCF-7 cells. Therefore we suggest that RVS can use as a novel class of anti-cancer drugs.

• Asian Pacific Journal of Cancer Prevention
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• 제14권10호
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• pp.5719-5723
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• 2013

Pharmacological and preventive properties of Petroselinum sativum seed extracts are well known, but the anticancer activity of alcoholic extracts and oil of Petroselinum sativum seeds on human breast cancer cells have not been explored so far. Therefore, the present study was designed to investigate the cytotoxic activities of these extracts against MCF-7 cells. Cells were exposed to 10 to $1000{\mu}g/ml$ of alcoholic seed extract (PSA) and seed oil (PSO) of Petroselinum sativum for 24 h. Post-treatment, percent cell viability was studied by 3-(4, 5-dimethylthiazol-2yl)-2, 5-biphenyl tetrazolium bromide (MTT) and neutral red uptake (NRU) assays, and cellular morphology by phase contrast inverted microscopy. The results showed that PSA and PSO significantly reduced cell viability, and altered the cellular morphology of MCF-7 cells in a concentration dependent manner. Concentrations of $50{\mu}g/ml$ and above of PSA and $100{\mu}g/ml$ and above of PSO were found to be cytotoxic in MCF-7 cells. Cell viability at 50, 100, 250, 500 and $1000{\mu}g/ml$ of PSA was recorded as 81%, 57%, 33%, 8% and 5%, respectively, whereas at 100, 250, 500, and $1000{\mu}g/ml$ of PSO values were 90%, 78%, 62%, and 8%, respectively by MTT assay. MCF-7 cells exposed to 250, 500 and $1000{\mu}g/ml$ of PSA and PSO lost their typical morphology and appeared smaller in size. The data revealed that the treatment with PSA and PSO of Petroselinum sativum induced cell death in MCF-7 cells.

• Asian Pacific Journal of Cancer Prevention
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• 제15권20호
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• pp.8617-8622
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• 2014

The goal of this study was to establish paclitaxel resistant MCF-7 cells, as in vitro model, to identify the molecular mechanisms leading to acquired chemoresistance in breast cancer cells. Resistant cells were developed by stepwise increasing exposure to paclitaxel. Gene expression levels of Bax and Bcl-2 along with protein levels of caspase-8 and caspase-9 were evaluated in two resistant cell lines (MCF-7/Pac64 and MCF-7/Pac5 nM). Morphological modifications in paclitaxel resistance cells were examined by light microscopy and fluorescence activated cell sorting (FACS). As an important indicator of resistance to chemotheraputic agents, the Bcl-2/Bax ratio showed a significant increase in both MCF-7/Pac5nM and MCF-7/Pac 64nM cells (p<0.001), while caspase-9 levels were decreased (p<0.001) and caspase-8 was increased (p<0.001). FACS analysis demonstrated that MCF-7/Pac64 cells were smaller than MCF-7 cells with no difference in their granularity. Our results support the idea that paclitaxel induces apoptosis in a mitochondrial-dependent manner. Identifying breast cancer patients with a higher Bcl-2/Bax ratio and caspase 9 level and then inhibiting the activity of these proteins may improve the efficacy of chemotheraputic agents.

• 한국식품영양과학회지
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• 제36권7호
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• pp.825-831
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• 2007

당귀로부터 분리한 decursin을 환경호르몬에 의해 증식을 유도한 인체 유방암세포(MCF-7)에 처리한 후 그 억제효과를 조사하였다. 인체 유방암세포주인 MCF-7은 20, 40, 60, 80 및 100 ${\mu}g/mL$ 농도로 decursin의 처리 시 20 ${\mu}g/mL$ 이상에서 농도 의존적으로 그 증식이 억제되었다. 호르몬이 제거된 배지로 배양한 세포에 0, 0.01, 0.1 및 1 ${\mu}M$의 농도로 환경 호르몬 $17{\beta}$-estradiol과 bisphenol을 처리한 결과 호르몬이 제거된 배지로 배양한 세포에 비해 세포의 증식을 유도하였으며, Yamada(21)와 본 실험 결과가 유사한 세포성장을 보여 암세포의 성장억제 효과를 측정하기 위한 환경호르몬의 농도를 0.1 ${\mu}M$로 하였다. 환경호르몬에 의해 증식이 유도된 MCF-7 세포에 당귀 메탄올추출물 및 decursin을 1, 3, 10 및 30 ${\mu}g/mL$ 농도로 처리한 결과 농도에 비례하여 세포의 증식을 억제하였으며, 10 ${\mu}g/mL$의 농도 이상에서는 대조구의 증식보다도 낮은 생존율을 나타내어 강한 세포독성을 나타내었다. 또한 hoechst 염색을 통하여 세포 핵의 변화를 알아본 결과 decursin 처리군에서 핵의 응축과 apoptic body가 관찰되어 decursin은 apoptosis를 유도함으로써 환경호르몬이 처리된 MCF-7 세포의 증식을 억제하는 것으로 판단된다. 이들 결과는 decursin이 환경호르몬에 의해 증식이 유도되는 MCF-7 세포의 성장을 apoptosis에 의해 억제한다는 것을 나타낸다.

• The Korean Journal of Physiology and Pharmacology
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• 제25권5호
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• pp.479-488
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• 2021

This study aimed to develop docetaxel (DTX) loaded poly(lactic-co-glycolic acid) (PLGA) nanoparticles (DTX-NPs) and to evaluate the different pharmacological sensitivity of NPs to MCF-7 and MDA-MB-231 breast cancer cells. NPs containing DTX or coumarin-6 were prepared by the nanoprecipitation method using PLGA as a polymer and d-α-tocopherol polyethylene glycol 1000 succinate (TPGS) as a surfactant. The physicochemical properties of NPs were characterized. In vitro anticancer effect and cellular uptake were evaluated in breast cancer cells. The particle size and zeta potential of the DTX-NPs were 160.5 ± 3.0 nm and -26.7 ± 0.46 mV, respectively. The encapsulation efficiency and drug loading were 81.3 ± 1.85% and 10.6 ± 0.24%, respectively. The in vitro release of DTX from the DTX-NPs was sustained at pH 7.4 containing 0.5% Tween 80. The viability of MDA-MB-231 and MCF-7 cells with DTX-NPs was 37.5 ± 0.5% and 30.3 ± 1.13%, respectively. The IC₅₀ values of DTX-NPs were 3.92- and 6.75-fold lower than that of DTX for MDA-MB-231 cells and MCF-7 cells, respectively. The cellular uptake of coumarin-6-loaded PLGA-NPs in MCF-7 cells was significantly higher than that in MDA-MB-231 cells. The pharmacological sensitivity in breast cancer cells was higher on MCF-7 cells than on MDA-MB-231 cells. In conclusion, we successfully developed DTX-NPs that showed a great potential for the controlled release of DTX. DTX-NPs are an effective formulation for improving anticancer effect in breast cancer cells.