scholarly journals Differential expression of genes in human normal and breast cancer cells determined by microarray technique

10.1038/14353 ◽  
1999 ◽  
Vol 23 (S3) ◽  
pp. 59-59
Author(s):  
Suxing Liu ◽  
Qun Wu ◽  
Paul Kirschmeier ◽  
Terri McClanahan ◽  
Johnathan Greene ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Differential Expression ◽  
Breast Cancer Cells ◽  
Expression Of Genes ◽  
Microarray Technique ◽  
Differential Expression Of Genes

scholarly journals The determination of changes in the expression of genes for selected specific transcriptional factors in in vitro ductal breast cancer cells under the influence of paclitaxel

2011 ◽  
Vol 16 (4) ◽  
Author(s):  
Marta Ziaja-Sołtys ◽  
Jolanta Rzymowska
Keyword(s):  
Breast Cancer ◽  
Cancer Therapy ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Transcriptional Factors ◽  
Breast Cancer Therapy ◽  
Ductal Breast Cancer ◽  
Expression Of Genes ◽  
Microarray Technique

AbstractThis study aimed to determine the changes in the expression of genes for selected specific transcriptional factors that have both activating and repressing functions in in vitro ductal breast cancer cells, under the influence of paclitaxel, applying the microarray technique. The cells are treated with 60 ng/ml and 300 ng/ml doses of paclitaxel that correspond to those applied in breast cancer therapy. About 60 ng/ml doses of paclitaxel cause a statistically significant increase in expression of all the 16 analysed genes coding transcriptional factors, ranging from 1.84-fold (for PO4F2) to 4.65-fold (for LMO4) (p < 0.05) in comparison with the control cells, and enhanced the taxane mechanism of action. The 300 ng/ml doses of paclitaxel cause a cytotoxic effect in the cells. In this article, we argue that these changes in gene expression values may constitute prognostic and predictive factors in ductal breast cancer therapy.

Differential expression and androgen regulation of microRNA molecules in breast cancer cells

2016 ◽  
Author(s):  
Mamoun Ahram ◽  
Rand Zaza ◽  
Ebtihal Mustafa ◽  
Heba Jarrar ◽  
Razan Al-Saber ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Differential Expression ◽  
Breast Cancer Cells ◽  
Androgen Regulation

Differential Expression of MiRNAs in Antiestrogen-Sensitive MCF-7vs.Antiestrogen-Resistant LY2 Breast Cancer Cells

2011 ◽  
pp. P3-68-P3-68
Author(s):  
Tissa T Manavalan ◽  
Yun Teng ◽  
Savitri N Appana ◽  
Susmita Datta ◽  
Theodore S Kalbfleisch ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Differential Expression ◽  
Breast Cancer Cells

scholarly journals Low doses of alpha particle irradiation modify the expression of genes regulating apoptosis in human MCF-7 breast cancer cells

2006 ◽  
Author(s):  
Jesús Soto ◽  
Carlos Sainz ◽  
Domingo González-Lamuño ◽  
Samuel Cos
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Alpha Particle ◽  
Breast Cancer Cells ◽  
Low Doses ◽  
Expression Of Genes ◽  
Particle Irradiation ◽  
Mcf 7

Collagen-induced differential expression of an RNA polymerase subunit by breast cancer cells

Biochimie ◽  
2005 ◽  
Vol 87 (8) ◽  
pp. 669-672 ◽  
Author(s):  
R SIRCHIA ◽  
C LUPARELLO
Keyword(s):  
Breast Cancer ◽  
Rna Polymerase ◽  
Cancer Cells ◽  
Differential Expression ◽  
Breast Cancer Cells

scholarly journals Differential expression of microRNA expression in tamoxifen-sensitive MCF-7 versus tamoxifen-resistant LY2 human breast cancer cells

2011 ◽  
Vol 313 (1) ◽  
pp. 26-43 ◽  
Author(s):  
Tissa T. Manavalan ◽  
Yun Teng ◽  
Savitri N. Appana ◽  
Susmita Datta ◽  
Theodore S. Kalbfleisch ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Differential Expression ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Microrna Expression ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Tamoxifen Resistant ◽  
Mcf 7

The Effect of a Newly Synthesized Ferrocene Derivative against MCF-7 Breast Cancer Cells and Spheroid Stem Cells through ROS Production and Inhibition of JAK2/STAT3 Signaling Pathway

2020 ◽  
Vol 20 (7) ◽  
pp. 875-886 ◽  
Author(s):  
Mitra Nourbakhsh ◽  
Shabnam Farzaneh ◽  
Adeleh Taghikhani ◽  
Afshin Zarghi ◽  
Shokoofe Noori
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Flow Cytometry ◽  
Stem Cell ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tetrazolium Salt ◽  
Ros Production ◽  
Expression Of Genes ◽  
Mcf 7

Background: Breast Cancer Stem Cells (BCSCs) possess the ability of self-renewal and cellular heterogeneity, and therefore, play a key role in the initiation, propagation and clinical outcome of breast cancer. It has been shown that ferrocene complexes have remarkable potential as anticancer drugs. Objective: The present study was conducted to investigate the effects of a novel ferrocene complex, 1- ferrocenyl-3-(4-methylsulfonylphenyl)propen-1-one (FMSP) on MCF-7 breast cancer cell line and its derived mammospheres with cancer stem cell properties. Methods: Mammospheres were developed from MCF-7 cells and validated by the evaluation of CD44 and CD24 cell surface markers by flow cytometry as well as of the expression of genes that are associated with stem cell properties by real-time PCR. Cells viability was assessed by a soluble tetrazolium salt (MTS) after the treatment of cells with various concentrations of FMSP. Apoptosis was evaluated by flow cytometry analysis of annexin V and PI labeling of cells. Reactive Oxygen Species (ROS) production was measured using a cellpermeable, oxidant-sensitive fluorescence probe (carboxy-H2DCFDA). The involvement of the JAK2/STAT3 pathway was also investigated by western blotting. Results: FMSP could successfully prevent mammosphere formation from differentiated MCF-7 cells and significantly down-regulated the expression of genes involved in the production of the stem cell properties including Wnt1, Notch1, β -catenin, SOX2, CXCR4 and ALDH1A1. FMSP decreased cell viability in both MCF-7 cells and spheroid cells, although MCF-10A cells were unaffected by this compound. Apoptosis was also dramatically induced by FMSP, via ROS production but independent of CD95 activation. Phosphorylation levels of JAK2 and STAT3 were also found to be significantly attenuated even in the presence of IL-6, the putative activator of the JAK/STAT pathway. Conclusion: FMSP can effectively target BCSCs via ROS production and modulation of major signaling pathways that contribute to the stemness of breast cancer cells, and therefore, might be considered a promising anticancer agent after in vivo studies.

scholarly journals miR-338-3p Is Regulated by Estrogens through GPER in Breast Cancer Cells and Cancer-Associated Fibroblasts (CAFs)

Cells ◽  
2018 ◽  
Vol 7 (11) ◽  
pp. 203 ◽  
Author(s):  
Adele Vivacqua ◽  
Anna Sebastiani ◽  
Anna Miglietta ◽  
Damiano Rigiracciolo ◽  
Francesca Cirillo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Cell Types ◽  
Cancer Associated Fibroblasts ◽  
Breast Cancer Patients ◽  
Expression Of Genes ◽  
Taqman Array

Estrogens acting through the classic estrogen receptors (ERs) and the G protein estrogen receptor (GPER) regulate the expression of diverse miRNAs, small sequences of non-coding RNA involved in several pathophysiological conditions, including breast cancer. In order to provide novel insights on miRNAs regulation by estrogens in breast tumor, we evaluated the expression of 754 miRNAs by TaqMan Array in ER-negative and GPER-positive SkBr3 breast cancer cells and cancer-associated fibroblasts (CAFs) upon 17β-estradiol (E2) treatment. Various miRNAs were regulated by E2 in a peculiar manner in SkBr3 cancer cells and CAFs, while miR-338-3p displayed a similar regulation in both cell types. By METABRIC database analysis we ascertained that miR-338-3p positively correlates with overall survival in breast cancer patients, according to previous studies showing that miR-338-3p may suppress the growth and invasion of different cancer cells. Well-fitting with these data, a miR-338-3p mimic sequence decreased and a miR-338-3p inhibitor sequence rescued the expression of genes and the proliferative effects induced by E2 through GPER in SkBr3 cancer cells and CAFs. Altogether, our results provide novel evidence on the molecular mechanisms by which E2 may regulate miR-338-3p toward breast cancer progression.

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