scholarly journals Bryostatin I inhibits growth of breast cancer cells through the inhibition of synuclein-A expression

2016 ◽  
Vol 11 (3) ◽  
pp. 615 ◽  
Author(s):  
Jun-Xia Sun ◽  
Yan Yan ◽  
Jian-Hong Xia ◽  
Li-Qing Zhou
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Video Clip ◽  
Inhibitory Effect ◽  
Oncostatin M ◽  
Cell Viability Assay ◽  
Viability Assay ◽  
Induced Apoptosis

<p class="Abstract">The present study was aimed to investigate the effect of bryostatin I on the expression of synuclein-A in breast cancer cells. Western blot analysis showed a significant (p&lt;0.005) reduction in the expression of synuclein-A from a concentration of 20 µM in H3922 cells. The inhibitory effect of bryostatin I on synuclein-A expression was further confirmed by the treatment of H3922 cells with known synuclein-A inhibitor, cytokine oncostatin M. Bryostatin I treatment of H3922 cells also significantly increased their sensitivity to the taxol. Incubation of the cells with 25 µM concentration of bryostatin I followed by treatment with 0.5 μM concentration of taxol induced apoptosis in 89% cells compared to 9% cells in the taxol alone treated cultures. Treatment of the H3922 cells with bryostatin I at 25 µM concentration led to a significant increase in the activation of histone H1 protein. The results from MTT assay showed a significant decrease in the cell viability from 10 µM concentration of bryostatin I. Thus, bryostatin I inhibits the growth of breast cancer cells through inhibition of synuclein-A expression and can be used for breast cancer treatment.</p><p><strong>Video Clip</strong></p><p><a href="https://youtube.com/v/VzeWcEMjrJA">Cell viability assay:</a> 5 min 14 sec </p>

scholarly journals Diosgenin Exerts Antitumor Activity via Downregulation of Skp2 in Breast Cancer Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Yanling Liu ◽  
Zijun Zhou ◽  
Jingzhe Yan ◽  
Xuefeng Wu ◽  
Guiying Xu
Keyword(s):  
Breast Cancer ◽  
Antitumor Activity ◽  
Cell Viability ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Underlying Mechanism ◽  
High Morbidity ◽  
Novel Approach ◽  
Transwell Invasion Assay ◽  
Induced Apoptosis

Background. Breast cancer is the common malignancy with high morbidity and mortality in women. S-phase kinase-associated protein 2 (Skp2) has been characterized to play an oncogenic role in the breast carcinogenesis and progression. Therefore, inactivation of Skp2 in breast cancer might be a novel approach for fighting breast malignancy. A natural compound diosgenin has been reported to exert anticancer activity in a variety of human cancers. However, the underlying mechanism has not been fully determined. Methods. In this study, we aim to explore whether diosgenin performed antitumor activity via inhibition of Skp2 in breast cancer cells using several methods including MTT, Transwell invasion assay, RT-PCR, western blotting, and transfection. Results. We found that diosgenin inhibited cell viability and stimulated apoptosis. Moreover, we found that diosgenin reduced cell invasion in breast cancer cells. Furthermore, diosgenin inhibited the expression of Skp2 in breast cancer cells. Notably, diosgenin reduced cell viability and motility and induced apoptosis via suppression of Skp2 in breast cancer cells. Conclusion. Our findings revealed that diosgenin could be a potential inhibitor of Skp2 for treating breast cancer.

scholarly journals Porous Cu-MOF Nanostructures with Anticancer Properties Prepared by a Controllable Ultrasound-Assisted Reverse Micelle Method

2021 ◽  
Author(s):  
Malihe Zeraati ◽  
Mohammadreza Moghaddam-Manesh ◽  
Sara Hosseinzadegan ◽  
Parya Kazemzadeh ◽  
Narendra Pal Singh Chauhan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Reverse Micelle ◽  
Breast Cancer Cells ◽  
Nitrogen Adsorption ◽  
Cell Viability Assay ◽  
Anticancer Properties ◽  
Viability Assay ◽  
Ultrasonic Assisted ◽  
Mcf 7

Abstract The ultrasonic assisted reverse micelle method was used to create Cu-MOF from Cu(NO3)2•3H2O and 2,6-pyridine dicarboxylic acid in a 1:1 molar proportion. It has been characterized using FT-IR, XRD, nitrogen adsorption analysis SEM and TEM-EDX. Cu-MOF has anticancer properties against MCF-7 breast cancer cells. Cytotoxicity testing was performed on MCF-7 breast cancer cells using the MTT cell viability assay, and cell proliferation and viability were found to be approximately 24 % higher than the control.

scholarly journals Noninvasive and Safe Cell Viability Assay for Breast Cancer MCF-7 Cells Using Natural Food Pigment

Biology ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 227
Author(s):  
Kyohei Yamashita ◽  
Ryoma Tagawa ◽  
Yoshikazu Higami ◽  
Eiji Tokunaga
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Living Cells ◽  
Natural Food ◽  
Cell Viability Assay ◽  
Viability Assay ◽  
A Cell ◽  
Reduced Nicotinamide Adenine Dinucleotide ◽  
Mcf 7

A dye exclusion test (DET) was performed to determine the viability of human breast cancer cells MCF-7, using natural food pigments as compared with trypan blue (TB), a typical synthetic dye for DET known to exhibit teratogenicity and cytotoxicity. We demonstrated that Monascus pigment (MP) is noninvasive to living cells and can effectively stain only dead cells. This study is the first verification of the applicability of MP to cancer cells. The appropriate MP concentration was 0.4% (0.02% as the concentration of pure MP) and all the dead cells were stained within 10 min. We found that the cell proliferation or the reduced nicotinamide adenine dinucleotide (NADH) activity of living cells was maintained over 48 h. Although 0.1% TB did not show an increase in dead cells, a marked decrease in NADH activity was confirmed. In addition, even when MP coexisted with cisplatin, staining of dead cells was maintained for 47 h, indicating stability to drugs (reagents). The cost of MP is estimated to be about 1/10 of TB. The fact that MP can be used as a cell viability determination reagent for Euglena and Paramecium, as shown in preceding papers, and also for MCF-7, as shown in this paper, indicates the possibility of application in more cells of different species.

HMPS (2-hydroxy-4-methoxyphenylstilbene), a stilbene derivative of rhapontigenin, and cell death by mitochondrial apoptotic pathway in breast cancer cells

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e22130-e22130
Author(s):  
J. Jung ◽  
H. Park ◽  
H. Jung ◽  
Y. Eun ◽  
J. Kim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cell Viability ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Recurrent Breast Cancer ◽  
Inhibitory Effect ◽  
Parp Cleavage ◽  
Recurrent Breast ◽  
Mcf 7

e22130 Background: Breast cancer with resistance to clinical therapy is a significant threat to live of recurrent breast cancer patients, and chemo-resistant breast cancer is increasing rapidly. During last several decades, natural stilbenoids have been studied on anticancer effects in vitro and in vivo, and resveratrol is the most famous stilbene as a leading compound in the studies of anticancer compounds derived from plants. HMPS (2-hydroxy-4-methoxyphenylstilbene) is an analogue derived from rhapontigenin (3,5,3'-trihydroxy-4'-methoxy-trans-stilbene), which is a stilbene of herbal plant Rheum undulatum. TMS (2,3',4,5'-tetramethoxystilbene), an another stilbene analogue from rhapontigenin, was reported potent anticancer effect on tamoxifen-resistant MCF-7 cells. In this study we investigated inhibitory effect of HMPS on proliferation of breast cancer and a potential for a new therapeutic candidate. Methods: We examined cell viability of MCF-7 and MDA-MB-231 by MTT assay after exposure to various concentrations of HMPS. Apoptotic cell death induced by HMPS was investigated by florescence microscopy, cell cycle analysis and western blotting. Results: Cell viability of breast cancer cells after 24 h exposure to HMPS decreased significantly, and both ER-positive and ER-negative breast cancer cells responded to HMPS. HMPS induced nucleus fragmentation and G2/M arrest followed by sub-G1 accumulation of apoptotic cells in time- and dose-dependent manner. During the process of cell death induced by HMPS, mitochondrial membrane potential was disturbed and caspase-3 and PARP cleavage were observed. Moreover, HMPS decreased cell number of LTED MCF-7 cells(Long term estradiol deprived cell) effectively. Conclusions: Our results demonstrates that proliferation inhibitory effect of HMPS is about 50-fold more potent than those of rhapontigenin and furthermore HMPS also inhibits cell growth of LTED cells which are difficult to treat therapeutic agents. Therefore, HMPS may be a potential therapeutic candidate to treat the recurrent breast cancer by alone or combination with other conventional anticancer agents. No significant financial relationships to disclose.

scholarly journals 4,6′-Anhydrooxysporidinone from Fusarium lateritium SSF2 Induces Autophagic and Apoptosis Cell Death in MCF-7 Breast Cancer Cells

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 869
Author(s):  
Dahae Lee ◽  
Sanghee Shim ◽  
Kisung Kang
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Neuronal Cell ◽  
Neuroprotective Effects ◽  
Cell Viability Assay ◽  
Viability Assay ◽  
Fusarium Lateritium ◽  
Caspase 7 ◽  
Mcf 7

Previous studies have reported that 4,6′-Anhydrooxysporidinone (SSF2-2), isolated from Fusarium lateritium SSF2, has neuroprotective effects on the HT-22 hippocampal neuronal cell line. However, the anti-cancer effect of SSF2-2 remains unclear. Here, we examined the viability of MCF-7 human breast cancer cells treated with SSF2-2 or left untreated using a cell viability assay kit. The underlying molecular mechanism was further investigated by Western blotting and immunocytochemistry studies. The results demonstrated that SSF2-2 inhibited the viability of MCF-7 cells. Treatment with SSF2-2 increased the levels of cleaved caspase-9, cleaved caspase-7, poly (ADP-ribose) polymerase (PARP), and LC3B. Additionally, SSF2-2 significantly increased the conversion of LC3-I to LC3II and LC3-positive puncta in MCF-7 cells.

scholarly journals Combined Luteolin and Indole-3-Carbinol Synergistically Constrains ERα-Positive Breast Cancer by Dual Inhibiting Estrogen Receptor Alpha and Cyclin-Dependent Kinase 4/6 Pathway in Cultured Cells and Xenograft Mice

Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2116
Author(s):  
Xiaoyong Wang ◽  
Lijuan Zhang ◽  
Qi Dai ◽  
Hongzong Si ◽  
Longyun Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Cultured Cells ◽  
Inhibitory Effect ◽  
Cyclin Dependent Kinase ◽  
Xenograft Mice ◽  
The Individual

The high concentrations of individual phytochemicals in vitro studies cannot be physiologically achieved in humans. Our solution for this concentration gap between in vitro and human studies is to combine two or more phytochemicals. We screened 12 phytochemicals by pairwise combining two compounds at a low level to select combinations exerting the synergistic inhibitory effect of breast cancer cell proliferation. A novel combination of luteolin at 30 μM (LUT30) and indole-3-carbinol 40 μM (I3C40) identified that this combination (L30I40) synergistically constrains ERα+ breast cancer cell (MCF7 and T47D) proliferation only, but not triple-negative breast cancer cells. At the same time, the individual LUT30 and I3C40 do not have this anti-proliferative effect in ERα+ breast cancer cells. Moreover, this combination L30I40 does not have toxicity on endothelial cells compared to the current commercial drugs. Similarly, the combination of LUT and I3C (LUT10 mg + I3C10 mg/kg/day) (IP injection) synergistically suppresses tumor growth in MCF7 cells-derived xenograft mice, but the individual LUT (10 mg/kg/day) and I3C (20 mg/kg/day) do not show an inhibitory effect. This combination synergistically downregulates two major therapeutic targets ERα and cyclin dependent kinase (CDK) 4/6/retinoblastoma (Rb) pathway, both in cultured cells and xenograft tumors. These results provide a solid foundation that a combination of LUT and I3C may be a practical approach to treat ERα+ breast cancer cells after clinical trials.

Lobetyolin inhibits the proliferation of breast cancer cells via ASCT2 down-regulation-induced apoptosis

2021 ◽  
pp. 096032712110214
Author(s):  
Yansong Chen ◽  
Ye Tian ◽  
Gongsheng Jin ◽  
Zhen Cui ◽  
Wei Guo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Glutamine Metabolism ◽  
Down Regulation ◽  
Anti Cancer ◽  
Induced Apoptosis ◽  
Glutamine Uptake

This study aimed to investigate the anti-cancer effect of lobetyolin on breast cancer cells. Lobetyolin was incubated with MDA-MB-231 and MDA-MB-468 breast cancer cells for 24 h. Glucose uptake and the mRNA expression of GLUT4 ( SLC2A4), HK2 and PKM2 were detected to assess the effect of lobetyolin on glucose metabolism. Glutamine uptake and the mRNA expression of ASCT2 ( SLC1A5), GLS1, GDH and GLUL were measured to assess the effect of lobetyolin on glutamine metabolism. Annexin V/PI double staining and Hoechst 33342 staining were used to investigate the effect of lobetyolin on cell apoptosis. Immunoblot was employed to estimate the effect of lobetyolin on the expression of proliferation-related markers and apoptosis-related markers. SLC1A5 knockdown with specific siRNA was performed to study the role of ASCT2 played in the anti-cancer effect of lobetyolin on MDA-MB-231 and MDA-MB-468 breast cancer cells. C-MYC knockdown with specific siRNA was performed to study the role of c-Myc played in lobetyolin-induced ASCT2 down-regulation. Myr-AKT overexpression was performed to investigate the role of AKT/GSK3β signaling played in lobetyolin-induced down-regulation of c-Myc and ASCT2. The results showed that lobetyolin inhibited the proliferation of both MDA-MB-231 and MDA-MB-468 breast cancer cells. Lobetyolin disrupted glutamine uptake via down-regulating ASCT2. SLC1A5 knockdown attenuated the anti-cancer effect of lobetyolin. C-MYC knockdown attenuated lobetyolin-caused down-regulation of ASCT2 and Myr-AKT overexpression reversed lobetyolin-caused down-regulation of both c-Myc and ASCT2. In conclusion, the present work suggested that lobetyolin exerted anti-cancer effect via ASCT2 down-regulation-induced apoptosis in breast cancer cells.

Notch4 Signaling Confers Susceptibility to TRAIL-Induced Apoptosis in Breast Cancer Cells

2015 ◽  
Vol 116 (7) ◽  
pp. 1371-1380 ◽  
Author(s):  
Shambhavi Naik ◽  
Marion MacFarlane ◽  
Apurva Sarin
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Induced Apoptosis
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