scholarly journals Abyssinone V-4′ Methyl Ether, a Flavanone Isolated from Erythrina droogmansiana, Exhibits Cytotoxic Effects on Human Breast Cancer Cells by Induction of Apoptosis and Suppression of Invasion

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Stéphane Zingue ◽  
Abel Joël Gbaweng Yaya ◽  
Julia Cisilotto ◽  
Larissa Vanelle Kenmogne ◽  
Emmanuel Talla ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Lines ◽  
Methyl Ether ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Cytotoxic Effects

Abyssinone V-4′ methyl ether (AVME) isolated from Erythrina droogmansiana was recently reported to exhibit anti-mammary tumor effect in mice. The present work was therefore aimed at elucidating its cellular and molecular mechanisms. To achieve our goal, the cytotoxicity of AVME against tumoral and non-tumoral cell lines was evaluated by resazurin reduction test; flow cytometry allowed us to evaluate the cell cycle and mechanisms of cell death; the mitochondrial transmembrane potential, reactive oxygen species (ROS) levels, and caspase activities as well as apoptosis-regulatory proteins (Bcl-2 and Bcl-XL) were measured in MDA-MB-231 cells. Further, the antimetastatic potential of AVME was evaluated by invasion assay. AVME exhibited cytotoxic effects in all tested tumor cell lines and induced a significant increase in the percentage of MDA-MB-231 cells at G2/M and S phases of the cell cycle in a concentration-dependent manner. AVME also induced apoptosis in MDA-MB-231 cells, which was accompanied by the activation of caspase-3 and caspase-9 and downregulation of Bcl-2 and Bcl-XL proteins. Moreover, AVME suppressed cancer cell invasion by the inhibition of the metalloproteinase-9 activity. Findings from this study suggest that AVME has anti-breast cancer activities expressed through mitochondrial proapoptotic pathway including impairment of aggressive behaviors of breast cancer cells.

Effect of new anti-neoplastic agent, MK615, from Japanese apricot, ume, on growth of breast cancer cells in vitro

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 11105-11105
Author(s):  
A. Nakagawa ◽  
T. Sawada ◽  
T. Okada ◽  
T. Ohsawa ◽  
M. Adachi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Breast Cancer Cell Lines ◽  
Dependent Manner ◽  
Japanese Apricot

11105 Background: MK615 is an extract mixture from Japanese apricot, UME. In this study, the anti-neoplastic effects of MK615 against breast cancer cells were investigated. Methods: Two breast cancer cell lines, MDA-MB-468 (MDA) and MCF7, were cultured with (600, 300, 150 μg/ml) or without MK615. After 72 hours of incubation, growth inhibition was evaluated by MTT assay, and the mechanism of the anti-neoplastic effect of MK615 was evaluated by cell cycle- and apoptosis assay. Results: MK615 inhibited the growth of MDA and MCF7 in a dose-dependent manner. The percentage growth inhibition of MDA at dosages of 600, 300, and 150 μg/ml was 59.2%, 52.4%, and 23.3%, respectively, and that for MCF7 was 83.5%, 52.7%, and 16.6%, respectively. Cell cycle analysis showed that MK615 increased the proportion of cells in G2-M phase in both MDA (7.8% to 11.7%) and MCF7 (8.1% to 18.7%), and finally both cell lines became apoptotic. The proportion of apoptotic cells increased with incubation time. Conclusions: MK615 effectively inhibits the growth of breast cancer cells in vitro, possibly by cell cycle modification and apoptosis induction. No significant financial relationships to disclose.

Momordica charantia Seed and Aryl Extracts Potentiate Growth Inhibition and Apoptosis by Dual Blocking of PI3K/AKT and MAPK Pathways as a Downstream Target of EGFR Signaling in Breast Cancer Cells

2020 ◽  
Vol 16 (5) ◽  
pp. 726-733
Author(s):  
Guzide Satir Basaran ◽  
Hatice Bekci ◽  
Ayse Baldemir ◽  
Selen Ilgun ◽  
Ahmet Cumaoglu
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Momordica Charantia ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Seed Extracts

Background and Objective: Herbal extracts and plant compounds are increasingly becoming of interest for their therapeutic potential in various cancer types. Momordica charantia is well known for its anti-diabetic, anti-inflammatory, and anti-cancer properties. Methods: In the present study, we investigated the antiproliferative and pro-apoptotic effects of Momordica charantia seed and aryl extracts on breast cancer cells and explored the underlying molecular mechanisms. Results: Our results showed that both extract significantly inhibited the growth of MCF-7 and MDA MB-231 cells in a concentration-dependent manner, and induced apoptosis by upregulation of caspase 9 and caspase 3 mRNA levels. In addition, in different incubation time, both extract evidently inhibited EGF and induced EGFR phosphorylation/activation in both cell lines. Moreover, Momordica charantia aryl and seed extracts inhibited phosphorylation/activation of PI3K/AKT and MAPK (ERK and P38) pathways in both cell lines. Conclusion: The current study clearly demonstrates that the Momordica charantia aryl and seed extracts have the potential to exert its cytotoxic effect on breast cancer cells by a mechanism involving inhibition of EGFR and EGRF related pathways with the induction of apoptosis. The overall finding demonstrates that this plant, especially seed extract, could be a potential source of new anticancer compounds for possible drug development against cancer.

scholarly journals Comparison of the effect of rhodium citrate-associated iron oxide nanoparticles on metastatic and non-metastatic breast cancer cells

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Natalia Lemos Chaves ◽  
Danilo Aquino Amorim ◽  
Cláudio Afonso Pinho Lopes ◽  
Irina Estrela-Lopis ◽  
Julia Böttner ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Human Tumor ◽  
Metastatic Breast ◽  
Cytotoxic Action ◽  
Dependent Manner ◽  
Metastatic Cells ◽  
Mcf 7

Abstract Background Nanocarriers have the potential to improve the therapeutic index of currently available drugs by increasing drug efficacy, lowering drug toxicity and achieving steady-state therapeutic levels of drugs over an extended period. The association of maghemite nanoparticles (NPs) with rhodium citrate (forming the complex hereafter referred to as MRC) has the potential to increase the specificity of the cytotoxic action of the latter compound, since this nanocomposite can be guided or transported to a target by the use of an external magnetic field. However, the behavior of these nanoparticles for an extended time of exposure to breast cancer cells has not yet been explored, and nor has MRC cytotoxicity comparison in different cell lines been performed until now. In this work, the effects of MRC NPs on these cells were analyzed for up to 72 h of exposure, and we focused on comparing NPs’ therapeutic effectiveness in different cell lines to elect the most responsive model, while elucidating the underlying action mechanism. Results MRC complexes exhibited broad cytotoxicity on human tumor cells, mainly in the first 24 h. However, while MRC induced cytotoxicity in MDA-MB-231 in a time-dependent manner, progressively decreasing the required dose for significant reduction in cell viability at 48 and 72 h, MCF-7 appears to recover its viability after 48 h of exposure. The recovery of MCF-7 is possibly explained by a resistance mechanism mediated by PGP (P-glycoprotein) proteins, which increase in these cells after MRC treatment. Remaining viable tumor metastatic cells had the migration capacity reduced after treatment with MRC (24 h). Moreover, MRC treatment induced S phase arrest of the cell cycle. Conclusion MRC act at the nucleus, inhibiting DNA synthesis and proliferation and inducing cell death. These effects were verified in both tumor lines, but MDA-MB-231 cells seem to be more responsive to the effects of NPs. In addition, NPs may also disrupt the metastatic activity of remaining cells, by reducing their migratory capacity. Our results suggest that MRC nanoparticles are a promising nanomaterial that can provide a convenient route for tumor targeting and treatment, mainly in metastatic cells.

scholarly journals Toxicological Effects of Traumatic Acid and Selected Herbicides on Human Breast Cancer Cells: In Vitro Cytotoxicity Assessment of Analyzed Compounds

Molecules ◽  
2019 ◽  
Vol 24 (9) ◽  
pp. 1710 ◽  
Author(s):  
Agata Jabłońska-Trypuć ◽  
Urszula Wydro ◽  
Elżbieta Wołejko ◽  
Andrzej Butarewicz
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Breast Cancer Cell Lines ◽  
Dependent Manner ◽  
Food Contaminants ◽  
Food Ingredient ◽  
Concentration Dependent Manner ◽  
Traumatic Acid

The main consequence of herbicides use is the presence of their residues in food of plant origin. A growing body of evidence indicates that herbicides cause detrimental effects upon human health while demonstrating a direct link of pesticides exposure with the occurrence of human chronic diseases, including cancer. There is a pressing need to develop our knowledge regarding interactions of food contaminants and food components both in vitro and in vivo. Pesticides are highly undesirable food contaminants, and traumatic acid (TA) is a very beneficial food ingredient, therefore we decided to study if TA may act as a compound that delays the stimulatory effect of pesticides on breast cancer cells. To analyze the potential effects that selected herbicides (MCPA, mesotrione, bifenox and dichlobenil) may have upon cancerous cells, we conducted studies of the cytotoxicity of physiological concentrations of four pesticides and the mix of TA with tested herbicides in three different breast cancer cell lines (MCF-7, ZR-75-1 and MDA-MB-231) and one normal healthy breast cell line MCF-12A. Based on the obtained results we conclude that TA in a concentration-dependent manner might influence selected effects of the studied herbicides for particular cancer cells lines.

scholarly journals Global transcriptome analysis reveals partial estrogen-like effects of karanjin in MCF-7 breast cancer cells

2021 ◽  
Author(s):  
Gaurav Bhatt ◽  
Akshita Gupta ◽  
Latha Rangan ◽  
Anil Mukund Limaye
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Target Genes ◽  
Biological Activities ◽  
Biological Effects ◽  
Dependent Manner ◽  
Cell Type ◽  
Concentration Dependent Manner ◽  
Mcf 7

Karanjin, an abundantly occurring furanoflavonoid in edible and non-edible legumes, exerts diverse biological effects in vivo, and in vitro. Its potential as an anticancer agent is also gaining traction following recent demonstrations of its anti-proliferative, cell cycle inhibitory, and pro-apoptotic effects. However, the universality of its anticancer potential is yet to be scrutinized, particularly so because flavonoids can act as selective estrogen receptor modulators (SERMs). Even the genomic correlates of its biological activities are yet to be examined in hormone responsive cells. This paper presents the early and direct transcriptomic footprint of 10 μM karanjin in MCF-7 breast cancer cells, using next generation sequencing technology (RNA-seq). We show that karanjin-modulated gene-expression repertoire is enriched in several hallmark gene sets, which include early estrogen-response, and G2/M checkpoint genes. Genes modulated by karanjin overlapped with those modulated by 1 nM 17β-estradiol (E2), or 1 μM tamoxifen. Karanjin altered the expression of selected estrogen-regulated genes in a cell-type, and concentration dependent manner. It downmodulated the expression of ERα protein in MCF-7 cells. Furthermore, ERα knockdown negatively impacted karanjins ability to modulate the expression of selected E2 target genes. Our data suggest that karanjin exerts its effects on ERα-positive breast cancer cells, at least in part, via ERα. The apparent SERM-like effects of karanjin pose a caveat to the anticancer potential of karanjin. In-depth studies on cell-type and concentration-dependent effects of karanjin may bring out its true potential in endocrine therapies.

scholarly journals Sialic acid-binding lectin-modified fructose-coated nanoparticles: a promising targeted therapeutic synthetic for breast cancers

2020 ◽  
Author(s):  
Lin He ◽  
Biyuan Zhang ◽  
Yuhua Song ◽  
Haiji Wang
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Breast Cancer Cell Lines ◽  
Multiple Drug ◽  
Her2 Overexpression ◽  
Coated Nanoparticles

Abstract Background: Sialic acid-binding lectin (cSBL) specifically kills tumor cells rather than healthy cells. Glycopolymer-coated nanoparticles are selectively ingested by tumor cells because they can interact with the enriched carbohydrate receptors located on the surface of tumor cells. In this context, we synthesized cSBL-modified fructose-coated nanoparticles (LMFN) and cSBL-modified glucose-coated nanoparticles (LMGN) to investigate their anticancer activity in various molecular subtypes of breast cancer cell lines. Methods: The syntheses of fructose-coated nanoparticles and glucose-coated nanoparticles were based on the chemicals of 1,2:4,5-di- O -isopropylidene- β -d-fructopyranose and 1,2:4,5-di- O -isopropylidene- β -d-glucopyranose, respectively. The carbodiimide-based method was employed to synthesize LMFN and LMGN. The antitumor mechanism was explored by cell cycle analysis with flowcytometry and the antitumor activity was assessed by cytotoxicity assay and multiple drug effects analysis. Results: The cytotoxicity assay showed that LMFN had robust antitumor activity against all breast cancer phenotype cell lines whereas LMGN was rarely efficacious to against human epidermal growth factor receptor 2-positive/overexpression (HER2+/overexpression) breast cancer cells. The intrinsic reason for these findings was that the overexpression of fructose transporter, GLUT5, was observed in all breast cancer subtype cell lines but only a paucity of glucose transporter, GLUT1, was expressed in HER2+/overexpression breast cancer cell lines that dampened the uptake of LMGN to these cells. The cell cycle analysis indicated that the anticancer activity of LMFN was achieved by arresting cell cycle in S phase. The multiple drug effects analysis suggested the synergistic effect in the combinations of LMFN and tamoxifen to kill estrogen receptor+ breast cancer cells and LMFN and trastuzumab to kill HER2+/overexpressed breast cancer cells. Conclusion: Our work pinpoints that LMFN may be a new-onset selection for molecularly targeted therapy of breast cancers and paves the way for establishing its clinical application in the future.

Apigenin Inhibits Growth of Breast Cancer Cells: The Role of ERα and HER2/neu

Acta Naturae ◽  
2015 ◽  
Vol 7 (3) ◽  
pp. 133-139 ◽  
Author(s):  
A. M. Scherbakov ◽  
O. E. Andreeva
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cells ◽  
Cancer Cell Lines ◽  
Luciferase Reporter ◽  
Her2 Positive ◽  
Cytotoxic Effects ◽  
High Doses

Phytoestrogens are a group of plant-derived compounds with an estrogen-like activity. In mammalians, phytoestrogens bind to the estrogen receptor (ER) and participate in the regulation of cell growth and gene transcription. There are several reports of the cytotoxic effects of phytoestrogens in different cancer cell lines. The aim of this study was to measure the phytoestrogen activity against breast cancer cells with different levels of ER expression and to elucidate the molecular pathways regulated by the leader compound. Methods used in the study include immunoblotting, transfection with a luciferase reporter vector, and a MTT test. We demonstrated the absence of a significant difference between ER+ and ER- breast cancer cell lines in their response to cytotoxic stimuli: treatment with high doses of phytoestrogens (apigenin, genistein, quercetin, naringenin) had the same efficiency in ER-positive and ER-negative cells. Incubation of breast cancer cells with apigenin revealed the highest cytotoxicity of this compound; on the contrary, naringenin treatment resulted in a low cytotoxic activity. It was shown that high doses of apigenin (50 М) do not display estrogen-like activity and can suppress ER activation by 17-estradiol. Cultivation of HER2-positive breast cancer SKBR3 cells in the presence of apigenin resulted in a decrease in HER2/neu expression, accompanied by cleavage of an apoptosis substrate PARP. Therefore, the cytotoxic effects of phytoestrogens are not associated with the steroid receptors of breast cancer cells. Apigenin was found to be the most effective phytoestrogen that strongly inhibits the growth of breast cancer cells, including HER2-positive ones.

scholarly journals Negative regulation of CDC42 expression and cell cycle progression by miR-29a in breast cancer

Open Medicine ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. 78-82 ◽  
Author(s):  
Mingliang Zhang ◽  
Wei Guo ◽  
Jun Qian ◽  
Benzhong Wang
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Real Time ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Cell Cycle Progression ◽  
Negative Regulation ◽  
Luciferase Assay ◽  
Cycle Progression

AbstractObjectiveThe inhibitory role of microRNA-29a (miR-29a) has been assessed in breast cancer cells. Herein, we analyze the underlying mechanisms of its role in cell cycle progression in breast cancer cells.MethodsWe applied real-time polymerase chain reaction (PCR) to detect the expression of miR-29 in breast cancer cell lines. Then one of the cell lines, MDA-MB-453, was transfected with mimics of miR-29a. The cell cycle was analyzed by fluorescence-activated cell sorting after staining the cells with propidium iodide. Real-time PCR, luciferase assay and western blot were used together to verify the regulation of the predicted target, cell division cycle 42 (CDC42) by miR-29a.ResultsMiR-29s were decreased in our selected mammary cell lines, among which miR-29a was the dominant isoform. Overexpression of miR-29a caused cell cycle arrest at the G0/G1 phase. We further found that miR-29a could target the expression of CDC42, which is a small GTPase associated with cell cycle progression.ConclusionWe suggest that miR-29a exerts its tumor suppressor role in breast cancer cells partially by arresting the cell cycle through negative regulation of CDC42.

scholarly journals Adipocytes Under Obese-Like Conditions Change Cell Cycle Distribution and Phosphorylation Profiles of Breast Cancer Cells: The Adipokine Receptor CAP1 Matters

2021 ◽  
Vol 11 ◽  
Author(s):  
Malin Bergqvist ◽  
Karin Elebro ◽  
Signe Borgquist ◽  
Ann H. Rosendahl
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Cell Cycle Distribution ◽  
Antibody Array ◽  
Er Positive ◽  
Metabolic Conditions

BackgroundObesity and associated metabolic conditions impact adipocyte functionality with potential consequences for breast cancer risk and prognosis, but contributing mechanisms remain to be understood. The adipokine receptor adenylyl cyclase-associated protein-1 (CAP1) has been implicated in the progression of breast cancer, but results are conflicting and the underlying molecular mechanisms are still unknown. In this study, molecular and cellular effects in breast cancer cells by stimulation of adipocytes under normal or obese-like conditions, and potential involvement of CAP1, were assessed.Material and MethodsEstrogen receptor (ER)-positive T47D and ER-negative MDA-MB-231 breast cancer cells were exposed to adipocyte-secretome from adipocytes placed under pressures mimicking normal and obese-like metabolic conditions. Changes in phosphorylated kinase proteins and related biological pathways were assessed by phospho-antibody array and PANTHER analysis, cell proliferation were investigated through sulforhodamine B, cell cycle distribution by flow cytometry. Functional effects of CAP1 were subsequently examined following small interfering (si)RNA-mediated knockdown.ResultsProtein phosphorylations involved in important biological processes were enriched in T47D breast cancer cells in response to adipocyte secretome from obese-like compared with normal conditions. The obesity-associated adipocyte secretome further stimulated cell proliferation and a shift from cell cycle G1-phase to S- and G2/M-phase was observed. Silencing of CAP1 decreased cell proliferation in both T47D and MDA-MB-231 cells, and reduced the obesity-associated secretome-induction of phosphoproteins involved in cell proliferation pathways.ConclusionsThese results indicate that the adipocyte secretome and CAP1 are mechanistically important for the proliferation of both ER-positive and ER-negative breast cancer cells, and potential signaling mediators were identified. These studies provide biological insight into how obesity-associated factors could affect breast cancer.

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