Vitamin D Growth Inhibition of Breast Cancer Cells: Gene Expression Patterns Assessed by cDNA Microarray

2003 ◽  
Vol 80 (1) ◽  
pp. 49-62 ◽  
Author(s):  
Srilatha Swami ◽  
Nalini Raghavachari ◽  
Uwe R. Muller ◽  
Yijia P. Bao ◽  
David Feldman
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Vitamin D ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Cdna Microarray ◽  
Breast Cancer Cells ◽  
Expression Patterns ◽  
Gene Expression Patterns

Chronic moderate ethanol intake differentially regulates vitamin D hydroxylases gene expression in kidneys and xenografted breast cancer cells in female mice

2017 ◽  
Vol 173 ◽  
pp. 148-156 ◽  
Author(s):  
Janice García-Quiroz ◽  
Rocío García-Becerra ◽  
Galia Lara-Sotelo ◽  
Euclides Avila ◽  
Sofía López ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Vitamin D ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Ethanol Intake ◽  
Female Mice

scholarly journals Integrative analysis of gene expression patterns predicts specific modulations of defined cell functions by estrogen and tamoxifen in MCF7 breast cancer cells

2005 ◽  
Vol 34 (1) ◽  
pp. 61-75 ◽  
Author(s):  
F Gadal ◽  
A Starzec ◽  
C Bozic ◽  
C Pillot-Brochet ◽  
S Malinge ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Cycle ◽  
Data Analysis ◽  
Differential Expression ◽  
Breast Cancer Cells ◽  
Cell Cycle Progression ◽  
Expression Patterns ◽  
Gene Expression Patterns ◽  
Cycle Progression

To explore the mechanisms whereby estrogen and antiestrogen (tamoxifen (TAM)) can regulate breast cancer cell growth, we investigated gene expression changes in MCF7 cells treated with 17β-estradiol (E2) and/or with 4-OH-TAM. The patterns of differential expression were determined by the ValiGen Gene IDentification (VGID) process, a subtractive hybridization approach combined with microarray validation screening. Their possible biologic consequences were evaluated by integrative data analysis. Over 1000 cDNA inserts were isolated and subsequently cloned, sequenced and analyzed against nucleotide and protein databases (NT/NR/EST) with BLAST software. We revealed that E2 induced differential expression of 279 known and 28 unknown sequences, whereas TAM affected the expression of 286 known and 14 unknown sequences. Integrative data analysis singled out a set of 32 differentially expressed genes apparently involved in broad cellular mechanisms. The presence of E2 modulated the expression patterns of 23 genes involved in anchors and junction remodeling; extracellular matrix (ECM) degradation; cell cycle progression, including G1/S check point and S-phase regulation; and synthesis of genotoxic metabolites. In tumor cells, these four mechanisms are associated with the acquisition of a motile and invasive phenotype. TAM partly reversed the E2-induced differential expression patterns and consequently restored most of the biologic functions deregulated by E2, except the mechanisms associated with cell cycle progression. Furthermore, we found that TAM affects the expression of nine additional genes associated with cytoskeletal remodeling, DNA repair, active estrogen receptor formation and growth factor synthesis, and mitogenic pathways. These modulatory effects of E2 and TAM upon the gene expression patterns identified here could explain some of the mechanisms associated with the acquisition of a more aggressive phenotype by breast cancer cells, such as E2-independent growth and TAM resistance.

scholarly journals Cooperation between BRCA1 and vitamin D is critical for histone acetylation of the p21waf1 promoter and for growth inhibition of breast cancer cells and cancer stem-like cells.

Oncotarget ◽  
2014 ◽  
Vol 5 (23) ◽  
pp. 11827-11846 ◽  
Author(s):  
Itay Pickholtz ◽  
Shira Saadyan ◽  
Gilmor I. Keshet ◽  
Victor S. Wang ◽  
Rachel Cohen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Vitamin D ◽  
Growth Inhibition ◽  
Histone Acetylation ◽  
Cancer Cells ◽  
Breast Cancer Cells

scholarly journals Stable Inhibition of Specific Estrogen Receptor α (ERα) Phosphorylation Confers Increased Growth, Migration/Invasion, and Disruption of Estradiol Signaling in MCF-7 Breast Cancer Cells

Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4144-4159 ◽  
Author(s):  
B. P. Huderson ◽  
T. T. Duplessis ◽  
C. C. Williams ◽  
H. C. Seger ◽  
C. G. Marsden ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Target Genes ◽  
Expression Patterns ◽  
Estrogen Receptor Α ◽  
Regulated Gene Expression ◽  
Mcf 7

Elevated phosphorylation of estrogen receptor α (ERα) at serines 118 (S118) and 167 (S167) is associated with favorable outcome for tamoxifen adjuvant therapy and may serve as surrogate markers for a functional ERα signaling pathway in breast cancer. It is possible that loss of phosphorylation at S118 and/or S167 could disrupt ERα signaling, resulting in aggressive ERα-independent breast cancer cells. To this end, MCF-7 breast cancer cells were stably transfected with an ERα-specific short hairpin RNA that reduced endogenous ERα. The resulting cell line was stably transfected with wild-type ERα (ER-AB cells), or ERα containing serine to alanine mutation at S118 or S167 (S118A cells and S167A cells, respectively). These stable cell lines expressed approximately equivalent ERα compared with parental MCF-7 cells and were evaluated for growth, morphology, migration/invasion, and ERα-regulated gene expression. S118A cells and S167A cells exhibited increased growth and migration/invasion in vitro. Forward- and side-scatter flow cytometry revealed that S167A cells were smaller in size, and both S118A and S167A cells exhibited less cellular complexity. S118A and S167A cells expressed pancytokeratin and membrane localization of β-catenin and did not express vimentin, indicating retention of epithelial lineage markers. Expression of ERα-target genes and other genes regulated by ERα signaling or involved in breast cancer were markedly altered in both S118A and S167A cells. In summary, attenuated phosphorylation of ERα at S118 and S167 significantly affected cellular physiology and behavior in MCF-7 breast cancer cells, resulting in increased growth, migration/invasion, compromised expression of ERα target genes, and markedly altered gene expression patterns.

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