Association of Sp3 and estrogen receptor α with the transcriptionally active trefoil factor 1 promoter in MCF-7 breast cancer cells

2008 ◽  
Vol 105 (2) ◽  
pp. 365-369 ◽  
Author(s):  
Lin Li ◽  
James R. Davie
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Estrogen Receptor Α ◽  
Trefoil Factor ◽  
Trefoil Factor 1 ◽  
Mcf 7

scholarly journals MicroRNA-27a Indirectly Regulates Estrogen Receptor α Expression and Hormone Responsiveness in MCF-7 Breast Cancer Cells

Endocrinology ◽  
2010 ◽  
Vol 151 (6) ◽  
pp. 2462-2473 ◽  
Author(s):  
Xiangrong Li ◽  
Susanne U. Mertens-Talcott ◽  
Shu Zhang ◽  
KyoungHyun Kim ◽  
Judith Ball ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Estrogen Receptor Α ◽  
Hormone Responsiveness ◽  
Mcf 7

scholarly journals The SMRT Coregulator Enhances Growth of Estrogen Receptor-α-Positive Breast Cancer Cells by Promotion of Cell Cycle Progression and Inhibition of Apoptosis

Endocrinology ◽  
2014 ◽  
Vol 155 (9) ◽  
pp. 3251-3261 ◽  
Author(s):  
Julia K. Blackmore ◽  
Sudipan Karmakar ◽  
Guowei Gu ◽  
Vaishali Chaubal ◽  
Liguo Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
Estrogen Receptor Α ◽  
Breast Cancer Progression ◽  
Apoptotic Genes ◽  
Mcf 7

Abstract The SMRT coregulator functions as a dual coactivator and corepressor for estrogen receptor-α (ERα) in a gene-specific manner, and in several studies its elevated expression correlates with poor outcome for breast cancer patients. A specific role of SMRT in breast cancer progression has not been elucidated, but SMRT knock-down limits estradiol-dependent growth of MCF-7 breast cancer cells. In this study, small-interfering RNA (siRNA) and short-hairpin RNA (shRNA) approaches were used to determine the effects of SMRT depletion on growth of ERα-positive MCF-7 and ZR-75–1 breast cancer cells, as well as the ERα-negative MDA-MB-231 breast cancer line. Depletion of SMRT inhibited growth of ERα-positive cells grown in monolayer but had no effect on growth of the ERα-negative cells. Reduced SMRT levels also negatively impacted the anchorage-independent growth of MCF-7 cells as assessed by soft agar colony formation assays. The observed growth inhibitions were due to a loss of estradiol-induced progression through the G1/S transition of the cell cycle and increased apoptosis in SMRT-depleted compared with control cells. Gene expression analyses indicated that SMRT inhibits apoptosis by a coordinated regulation of genes involved in apoptosis. Functioning as a dual coactivator for anti-apoptotic genes and corepressor for pro-apoptotic genes, SMRT can limit apoptosis. Together these data indicate that SMRT promotes breast cancer progression through multiple pathways leading to increased proliferation and decreased apoptosis.

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