• Journal of Physiology & Pathology in Korean Medicine
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• v.28 no.3
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• pp.310-316
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• 2014

Oldenlandia diffusa, Cremastra appendiculata and Fritillaria thunbergii are widely distributed in the Korea, China and Japan, and has been used in traditional medicine for various diseases, such as pharyngolaryngitis, tonsillitis, goiter and stomach ulcer. However, the anti-cancer activities in human breast cancer have not been clearly elucidated yet. In this study, it was compared the in vitro cytotoxic effects of single and complex treatment of O. diffusa, C. appendiculata and F. thunbergii. We treat human breast cancer MCF-7 cells with O. diffusa, C. appendiculata and F. thunbergii. And we evaluated viability, growth inhibition, morphological changes, apoptotic bodies formation, measurement of the cell cycle and formation of DNA fragmentation of these cells. It was found that single treatment of O. diffusa could inhibit the cell proliferation in human breast cancer MCF-7 cells. However, complex treatment of O. diffusa, C. appendiculata and F. thunbergii is weakly or not affect the cell proliferation of MCF-7 cells. And anti-proliferative effects of O. diffusa in MCF-7 cells was associated with G1 arrest of cell cycle. These findings suggest that O. diffusa may be a potential chemotherapeutic agent for the control of human breast cancer cells and further studies will be needed to identify the molecular mechanisms.

• 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.

• 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.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.18
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• pp.8445-8450
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• 2016

Background: Breast cancer is the most common neoplasm in women and the most frequent cause of death in those between 35 and 55 years of age. All multicellular organisms have an innate immune system, whereas the adaptive or 'acquired' immune system is restricted to vertebrates. This study focused on the effect of conditioned medium isolated from cultured breast cancer cells on NB4 neutrophil-like cells. Materials and Methods: In the current study neutrophil-like NB4 cells were incubated with MCF-7 cell-conditioned medium. After 6 h incubation the intracellular receptor TLR2, was analyzed. Results: The results revealed that MCF-7 cell-conditioned medium elicited expression of TLR2 in NB4 cells. Conclusions: This treatment would result in the production of particular stimulants (i.e. soluble cytokines), eliciting the expression of immune system receptors. Furthermore, the flow cytometry results demonstrated that MCF-7 cell-conditioned medium elicited an effect on TLR2 intracellular receptors.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6233-6237
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• 2012

Survivin, a new member of the inhibitor of apoptosis protein (IAP) family, both inhibits apoptosis and regulates the cell cycle. It is overexpressed in breast tumor tissues. In this study, we designed two survivin specific DNAzymes (DRz1 and DRz2) targeting survivin mRNA. The results showed that DRz1 could decrease the expression of survivin by nearly 60%. Furthermore, DRz1 significantly inhibited cell proliferation, induced apoptosis and inhibited migration in MCF-7 cells. In addition, down-regulation of survivin expression was associated with increased caspase-3 and -9 activities in MCF-7 cells after 24 h transfection. In our experiments, the efficacy of DRz1 to influence survivin levels and associated effects were better than DRz2. Survivin-DRz1 might have anti-tumorigenic activity and may potentially provide the basis for a novel therapeutic intervention in breast cancer treatment.

• Biomolecules & Therapeutics
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• v.26 no.3
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• pp.328-334
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• 2018

Because of the unsatisfactory treatment options for breast cancer (BC), there is a need to develop novel therapeutic approaches for this malignancy. One such strategy is chemotherapy using non-toxic dietary substances and botanical products. Studies have shown that Panduratin A (PA) possesses many health benefits, including anti-inflammatory, anti-bacterial, anti-oxidant and anticancer activities. In the present study, we provide evidence that PA treatment of MCF-7 BC cells resulted in a time- and dose-dependent inhibition of cell growth with an $IC_{50}$ of $15{\mu}M$ and no to little effect on normal human MCF-10A breast cells. To define the mechanism of these anti-proliferative effects of PA, we determined its effect critical molecular events known to regulate the cell cycle and apoptotic machinery. Immunofluorescence and flow cytometric analysis of Annexin V-FITC staining provided evidence for the induction of apoptosis. PA treatment of BC cells resulted in increased activity/expression of mitochondrial cytochrome C, caspases 7, 8 and 9 with a significant increase in the Bax:Bcl-2 ratio, suggesting the involvement of a mitochondrial-dependent apoptotic pathway. Furthermore, cell cycle analysis using flow cytometry showed that PA treatment of cells resulted in G0/G1 arrest in a dose-dependent manner. Immunoblot analysis data revealed that, in MCF-7 cell lines, PA treatment resulted in the dose-dependent (i) induction of $p21^{WAF1/Cip1}$ and p27Kip1, (ii) downregulation of Cyclin dependent kinase (CDK) 4 and (iii) decrease in cyclin D1. These findings suggest that PA may be an effective therapeutic agent against BC.

• The Journal of Korean Obstetrics and Gynecology
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• v.28 no.2
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• pp.26-39
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• 2015

Objectives : Dendropanax morbifera is known as a tree that has been used in traditional medicine for various diseases. However, its biological activities in cancer have not yet been clearly elucidated. In this study, we investigated the anti-cancer effects of water extract of Dendropanax morbifera (DP) on 2 human breast cancer cell lines (estrogen dependent MCF-7 and estrogen independent MDA-MB-231). Methods : The MTT assay and flow cytometry were used to assess cell proliferation, along with cell cycle analysis. Nitric oxide production was detected by Griess assay. The expression of apoptosis related gene was assessed by quantitative real-time PCR. Results : Our data revealed that DP inhibits the cell growth in a dose dependent manner (0, 50, 100, 250, and 500 μg/ml) of both estrogen independent MDA-MB-231 and estrogen dependent MCF-7 breast cancer cells. Also, LPS induced nitric oxide production was significantly reduced by DP. Cell cycle analysis showed an increased G1 phase in the MCF-7 cell and G2/M phase in the MDA-MB-231 cell. DP decreased mRNA expression of apoptotic suppressor gene Bcl-xL, and increased mRNA expression of pro-apoptotic genes. DP increased mRNA expression of p21, and Rip1 in both cell. And DP decreased mRNA expression of survivin in the MCF-7 cell. Conclusions : Taken together, these results indicate that DP extract are source of anti-cancer potential and could be developed botanical drug.

• 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.

• Archives of Pharmacal Research
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• v.20 no.6
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• pp.572-578
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• 1997

To gain further insight into how antiestrogens modulate cell function, the effects of antiestrogen on cell proliferation were studied in human breast cancer cells. We examined the effects of trans-tamoxifen on the proliferation of three human breast cancer cell lines that differed in their estrogen receptor contents. Trans-tamoxifen $(1{\mu}M)$ markedly inhibited the estrogen stimulated proliferation of MCF-7 human breast cancer cells that contained high levels of estrogen receptor $(1.15{\pm}0.03 pmole/mg protein)$ over that of control. In T47D cells that contained low levels of estrogen receptor $(0.23{\pm}0.05 pmole/mg protein)$, trans-tamoxifen $(1{\mu}M)$ showed minimal inhibition of estrogen stimulated cell proliferation over that of control. MDA-MB-231 cells, that contained no detectable levels of estrogen receptors, had their growth unaffected by trans-tamoxifen treatment. These results showed their sensitivity to growth inhibition by antiestrogen conrrelated well with their estrogen receptor content. Also we examined the effect of antiestrogen on cellular progestrone receptor level as well as plasminogen activator activity in MCF-7 cells. Trans-tamoxifen $(1{\mu}M)$ showed maximal inhibition of estrogen stimulated progestrone receptor level as well as plasminogen activator activity in MCF-7 cells that were stimulated by estrogen. It is not clear whether these inhibitions of progestrone receptor and plasminogen activator activity by estrogen are related to the antiestrogen inhibition of cell proliferation of MCF-7 cells. From the results of this study, it is clearly demonstrated that trans-tamoxifen is an antiestrogen in MCF-7 human breast cancer cells. Our data suggest that the biological effectiveness of trans-tamoxifen appear to result from its affinity of interaction with the estrogen receptor.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.1
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• pp.273-276
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• 2014

Ellagic acid has been shown to inhibit tumor cell growth. However, the underlying molecular mechanisms remain elusive. In this study, our aim was to investigate whether ellagic acid inhibits the proliferation of MCF-7 human breast cancer cells via regulation of the TGF-${\beta}$/Smad3 signaling pathway. MCF-7 breast cancer cells were transfected with pEGFP-C3 or pEGFP-C3/Smad3 plasmids, and treated with ellagic acid alone or in combination with SIS3, a specific inhibitor of Smad3 phosphorylation. Cell proliferation was assessed by MTT assay and the cell cycle was detected by flow cytometry. Moreover, gene expression was detected by RT-PCR, real-time PCR and Western blot analysis. The MTT assay showed that SIS3 attenuated the inhibitory activity of ellagic acid on the proliferation of MCF-7 cells. Flow cytometry revealed that ellagic acid induced G0/G1 cell cycle arrest which was mitigated by SIS3. Moreover, SIS3 reversed the effects of ellagic acid on the expression of downstream targets of the TGF-${\beta}$/Smad3 pathway. In conclusion, ellagic acid leads to decreased phosphorylation of RB proteins mainly through modulation of the TGF-${\beta}$/Smad3 pathway, and thereby inhibits the proliferation of MCF-7 breast cancer cells.