Oestrogen treatment enhances the sensitivity of hormone-resistant breast cancer cells to doxorubicin

2010 ◽  
Vol 31 (2) ◽  
pp. 137-143 ◽  
Author(s):  
Alexander M. Scherbakov ◽  
Yulia S. Lobanova ◽  
Olga E. Andreeva ◽  
Valentina A. Shatskaya ◽  
Mikhail A. Krasil'nikov
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Nuclear Factor Κb ◽  
Apoptotic Response ◽  
Oestrogen Treatment ◽  
Interfering Rna ◽  
Mcf 7 ◽  
Resistant Cells

Recently, it was shown that the resistance of breast cancer cells to growth-stimulating oestrogen action may be accompanied with the paradoxical tumour sensitization to oestrogen apoptotic action. In the present paper, we studied the influence of oestrogens on the sensitivity of resistant breast tumours to cytostatic drugs, and to evaluate the role of NF-κB (nuclear factor κB) signalling in the regulation of the apoptotic response of the resistant cells. The experiments were carried out on the oestrogen-dependent MCF-7 breast cancer cells and resistant MCF-7/LS subline generated through long-term cultivation of the parental cells in the absence of oestrogen. The cell treatment with the combination of oestradiol and Dox (doxorubicin) was found to enhance the apoptotic action of Dox in MCF-7/LS cells but not in the parent cells. MCF-7/LS cells were characterized by the increased level of ROS (reactive oxygen species) and decreased NF-κB activity. Oestradiol in combination with Dox leads to significant NF-κB stimulation and its accumulation in the nucleus of MCF-7/LS cells. The knockdown of NF-κB with siRNA (small interfering RNA) increased the apoptotic response of the MCF-7/LS cells to both Dox and oestradiol demonstrating the important role of NF-κB in the protection of the MCF-7/LS cells against apoptosis. In general, the results obtained show that: (i) oestradiol enhances the apoptotic action of Dox in the resistant breast cancer cells; and (ii) suppression of NF-κB signalling amplifies the apoptotic response of the resistant cells to both oestrogen and Dox, demonstrating that NF-κB may serve as a potential target in the therapy of the resistant breast cancer.

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

scholarly journals Unique Roles of p160 Coactivators for Regulation of Breast Cancer Cell Proliferation and Estrogen Receptor-α Transcriptional Activity

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1588-1596 ◽  
Author(s):  
Sudipan Karmakar ◽  
Estrella A. Foster ◽  
Carolyn L. Smith
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Breast Cancer Cells ◽  
Transcriptional Activity ◽  
Interfering Rna ◽  
Mcf 7

Each of the three members of the p160 steroid receptor coactivator (SRC) family of coactivators (SRC-1, SRC-2 and SRC-3) stimulates estrogen receptor (ER)-α function in trans-activation assays. Consequently, we sought to elucidate their contributions to the ER-regulated processes of cell proliferation, apoptosis, and the expression of ERα target genes in MCF-7 breast cancer cells. The small interfering RNA depletion of SRC-2 or SRC-3 but not SRC-1 inhibited growth of MCF-7 cells, and this was reflected in decreased cell cycle progression and increased apoptosis in SRC-2- or SRC-3-depleted cells as well as a reduction in ERα transcriptional activity measured on a synthetic reporter gene. However, only SRC-3 depletion blocked estradiol stimulated cell proliferation. Depletion of SRC-1 did not affect these events, and together this reveals functional differences between each of the three SRC family coactivators. Regulation of the endogenous ERα target gene, c-myc was not affected by depletion of any of the p160 coactivators although depletion of each of them decreased pS2 mRNA expression in estradiol-treated MCF-7 cells. Moreover, progesterone receptor and cyclin D1 gene expression were decreased in SRC-3 small interfering RNA-treated cells. Expression of mRNA and protein levels for the antiapoptotic gene, Bcl-2 was dependent on SRC-3 expression, whereas Bcl-2 protein but not mRNA expression also was sensitive to SRC-1 depletion. Together these data indicate that the closely related p160 coactivators are not functionally redundant in breast cancer cells because they play gene-specific roles in regulating mRNA and protein expression, and they therefore are likely to make unique contributions to breast tumorigenesis.

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.

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
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