scholarly journals d Rhamnose β-hederin reverses chemoresistance of breast cancer cells by regulating exosome-mediated resistance transmission

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Wei-xian Chen ◽  
Ling-yun Xu ◽  
Qi Qian ◽  
Xiao He ◽  
Wen-ting Peng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Target Gene ◽  
Gene Prediction ◽  
Docetaxel Resistance ◽  
Resistance Reversal ◽  
Mcf 7 ◽  
Chinese Medicinal Plant

d Rhamnose β-hederin (DRβ-H), an active component extracted from the traditional Chinese medicinal plant Clematis ganpiniana, has been reported to be effective against breast cancer. Recent studies have also indicated that the isolated exosomes (D/exo) from docetaxel-resistant breast cancer cells MCF-7 (MCF-7/Doc) were associated with resistance transmission by delivering genetic cargo. However, the relevance of D/exo during DRβ-H exposure remains largely unclear. In the present work, exosomes were characterized by morphology and size distribution. We reinforced the significant role of D/exo in spreading chemoresistance from MCF-7/Doc to recipient sensitive cells after absorption and internalization. DRβ-H could reduce the formation and release of D/exo. Next, we demonstrated that DRβ-H was able to reverse docetaxel resistance and that D/exo was responsible for DRβ-H-mediated resistance reversal. We also found that DRβ-H could decrease the expressions of several most abundant miRNAs (miR-16, miR-23a, miR-24, miR-26a, and miR-27a) transported by D/exo. Target gene prediction and pathway analysis showed the involvement of these selected miRNAs in pathways related to treatment failure. Our results suggested that DRβ-H could reduce D/exo secretion from MCF-7/Doc cells and induce the reduction in resistance transmission via D/exo.

scholarly journals The Cytotoxic Properties of Baeckea frutescens Branches Extracts in Eliminating Breast Cancer Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
S. H. Shahruzaman ◽  
M. F. Mustafa ◽  
S. Ramli ◽  
S. Maniam ◽  
S. Fakurazi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Glucose Uptake ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Glucose Consumption ◽  
Uptake Assay ◽  
Glucose Uptake Assay ◽  
Baeckea Frutescens ◽  
Mcf 7

Breast cancer is the leading cause of cancer death in women in over 100 countries worldwide and accounts for almost 1 in 4 cancer cases among women. Baeckea frutescens of the family Myrtaceae has been used in traditional medicine and is known to possess antibacterial, antipyretic, and cytoprotective properties. In this study, we investigated the role of Baeckea frutescens branches extracts against human breast cancer cells. Baeckea frutescens branches extracts were prepared using Soxhlet apparatus with solvents of different polarity. The selective cytotoxic activity and the glucose consumption rate of Baeckea frutescens branches extracts of various concentrations (20 to 160 ug/ml) at 24-, 48-, and 72-hour time points were studied using MTT and glucose uptake assay. The IC50 values in human breast cancer (MCF-7 and MDA-MB-231) and mammary breast (MCF10A) cell lines were determined. Apoptotic study using AO/PI double staining was performed using fluorescent microscopy. The glucose uptake was measured using 2-NBDG, a fluorescent glucose analogue. The phytochemical screening of major secondary metabolites in plants was performed. This study reports that Baeckea frutescens branches extracts showed potent selective cytotoxic activity against MCF-7 cells compared to MDA-MB-231 cells after 72 hours of treatment. Evidence of early apoptosis which includes membrane blebbing and chromatin condensation was observed after 72 hours of treatment with Baeckea frutescens branches extracts. Interestingly, for the glucose uptake assay, the inhibition was observed as early as 24 hours upon treatment. All Baeckea frutescens extracts showed the presence of major secondary metabolites such as tannin, triterpenoid, flavonoid, and phenol. However, alkaloid level was unable to be determined. The identification of Baeckea frutescens and its possible role in selectively inhibiting glucose consumption in breast cancer cells defines a new role of natural product that can be utilised as an effective agent that regulates metabolic reprogramming in breast cancer.

scholarly journals Knockdown of ICB-1 gene enhanced estrogen responsiveness of ovarian and breast cancer cells

2010 ◽  
Vol 17 (1) ◽  
pp. 147-157 ◽  
Author(s):  
Anna Konwisorz ◽  
Anette Springwald ◽  
Martina Haselberger ◽  
Regina Goerse ◽  
Olaf Ortmann ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Ovarian Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Chromosome 1 ◽  
Ovarian Cancer Cells ◽  
General Role ◽  
Estrogen Response ◽  
Mcf 7

ICB-1 chromosome 1 open reading frame 38 (C1orf38) is a human gene initially described by our group to be involved in differentiation processes of cancer cells. Recently, we have reported ICB-1 as a novel estrogen target gene and identified an estrogen response element in its promoter. In this study, we examined the role of ICB-1 in regulation of proliferation of breast and ovarian cancer cells. We knocked down its expression in estrogen-dependent MCF-7 breast cancer cells and hormone-unresponsive SK-OV-3 ovarian cancer cells by stable transfection with a specific shRNA plasmid followed by G-418 selection. Knockdown of ICB-1 enabled a considerable estrogen response of SK-OV-3 cells in terms of proliferation. This transformation of SK-OV-3 cells into an estrogen-responsive phenotype was accompanied by upregulation of estrogen receptor α (ERα) expression and a significant decrease of ERβ expression on the mRNA level. Expression of ERα-dependent genes progesterone receptor, pS2, fibulin 1c, and c-fos was elevated in SK-OV-3 cells stably expressing ICB-1 shRNA. In MCF-7 cells, ICB-1 knockdown exerted similar effects on gene expression, supporting a general role of ICB-1 in estrogen responsiveness. Our data suggest that differentiation-associated gene ICB-1 might exert antagonistic actions on cellular estrogen response, which can result in inhibition of estradiol-triggered proliferation. The molecular mechanisms mediating this inhibitory effect of ICB-1 on estrogen signaling are suggested to be limitation of ERα transcript levels but sustaining high levels of ERβ, reducing both activation of ERα target genes and cellular proliferation. The identification of ICB-1 as a new player in endocrine-related cancer encourages further studies on the significance of this gene in cancer development and therapy.

Epigallocatechin-3-gallate elicits Ca2+ spike in MCF-7 breast cancer cells: Essential role of Cav3.2 channels

Cell Calcium ◽  
2014 ◽  
Vol 56 (4) ◽  
pp. 285-295 ◽  
Author(s):  
Elia Ranzato ◽  
Valeria Magnelli ◽  
Simona Martinotti ◽  
Zeina Waheed ◽  
Stuart M. Cain ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Essential Role ◽  
Mcf 7

Role of specific apoptotic pathways in the restoration of paclitaxel-induced apoptosis by valspodar in doxorubicin-resistant MCF-7 breast cancer cells

2000 ◽  
Vol 59 (3) ◽  
pp. 231-244 ◽  
Author(s):  
Antony Chadderton ◽  
David J. Villeneuve ◽  
Stefan Gluck ◽  
Angie F. Kirwan-Rhude ◽  
Brian R. Gannon ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Apoptotic Pathways ◽  
Induced Apoptosis ◽  
Mcf 7

scholarly journals The Role of Peroxiredoxin II in Radiation-Resistant MCF-7 Breast Cancer Cells

2005 ◽  
Vol 65 (22) ◽  
pp. 10338-10346 ◽  
Author(s):  
Tieli Wang ◽  
Daniel Tamae ◽  
Thomas LeBon ◽  
John E. Shively ◽  
Yun Yen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Radiation Resistant ◽  
Mcf 7

Role of PDZ Domain-Containing 1 (PDZK1) in MCF-7 Breast Cancer Cells.

2009 ◽  
Vol 81 (Suppl_1) ◽  
pp. 365-365
Author(s):  
Jong G. Kim ◽  
Jihang Ju ◽  
Suresh K. Alahari ◽  
Hogyoung Kim
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Pdz Domain ◽  
Mcf 7

Characterization of tumor-induced platelet aggregation: The role of immunorelated GPIb and expression by MCF-7 breast cancer cells

1995 ◽  
Vol 79 (3) ◽  
pp. 261-274 ◽  
Author(s):  
Leslie Oleksowicz ◽  
Zbigniew Mrowiec ◽  
Edward Schwartz ◽  
Manoochehr Khorshidi ◽  
Janice P. Dutcher ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Platelet Aggregation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mcf 7

Induction of Apoptosis and Autophagy by Ternary Copper Complex Towards Breast Cancer Cells

2021 ◽  
Vol 21 ◽  
Author(s):  
Zheng Yang Lee ◽  
Chee Hong Leong ◽  
Krystal U Ling Lim ◽  
Christopher Chun Sing Wong ◽  
Pornwasu Pongtheerawan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Copper Complex ◽  
Breast Cancer Cells ◽  
Caspase 3 ◽  
Caspase 9 ◽  
Mcf 7

Background: Copper complex has been gaining much attention in anticancer research as targeted agent since cancer cells uptake more copper than non-cancerous cells. Our group has synthesised a ternary copper complex which is composed of 1,10-phenanthroline and tyrosine [Cu(phen)(L-tyr)Cl].3H20. These two payloads are designed to cleave DNA and inhibit protein degradation system (proteasome) concurrently in cancer cells, making this copper complex a dual-target compound. Objective: Current study was carried out to investigate the mode of cell death and role of autophagy induced by [Cu(phen)(L-tyr)Cl].3H20 in MCF-7 and MDA-MB-231 breast cancer cells. Methods: Growth inhibition of [Cu(phen)(L-tyr)Cl].3H20 towards MDA-MB-231 and human non-cancerous MCF10A breast cells was determined by MTT assay. Annexin-V-FITC/PI and cell cycle analysis were evaluated by flow cytometry. The expression of p53, Bax, caspase-9, caspase-7, caspase-3 and LC3 were determined using western blot analysis. The cells were then co-treated with hydroxychloroquine to ascertain the role of autophagy induced by [Cu(phen)(L-tyr)Cl].3H20. Results: [Cu(phen)(L-tyr)Cl].3H20 inhibited the growth of cancer cells dose-dependently with less toxicity towards MCF10A cells. Additionally, [Cu(phen)(L-tyr)Cl].3H20 induced apoptosis and cell cycle arrest towards MCF-7 and MDA-MB-231 breast cancer cells possibly via regulation of p53, Bax, caspase-9, caspase-3 and capase-7. The expression of LC3II was upregulated in both cancer cell lines upon treatment with [Cu(phen)(L-tyr) Cl].3H20, indicating the induction of autophagy. Co-treatment with autophagy inhibitor hydroxychloroquine significantly enhanced growth inhibition of both cell lines, suggesting that the autophagy induced by [Cu(phen)(L-tyr) Cl].3H20 in both breast cancer cells was promoting cell survival. Conclusion: [Cu(phen)(L-tyr)Cl].3H20 holds great potential to be developed for breast cancer treatment.

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