Overexpression of histone deacetylase HDAC1 modulates breast cancer progression by negative regulation of estrogen receptor ?

2003 ◽  
Vol 107 (3) ◽  
pp. 353-358 ◽  
Author(s):  
Hideki Kawai ◽  
Huchun Li ◽  
Shalom Avraham ◽  
Shuxian Jiang ◽  
Hava Karsenty Avraham
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Histone Deacetylase ◽  
Cancer Progression ◽  
Negative Regulation ◽  
Breast Cancer Progression

scholarly journals Estrogen Receptor (ER)α-regulated Lipocalin 2 Expression in Adipose Tissue Links Obesity with Breast Cancer Progression

2014 ◽  
Vol 290 (9) ◽  
pp. 5566-5581 ◽  
Author(s):  
Brian G. Drew ◽  
Habib Hamidi ◽  
Zhenqi Zhou ◽  
Claudio J. Villanueva ◽  
Susan A. Krum ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Adipose Tissue ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Lipocalin 2

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.

scholarly journals Protein Acetylation and Histone Deacetylase Expression Associated with Malignant Breast Cancer Progression

2009 ◽  
Vol 15 (9) ◽  
pp. 3163-3171 ◽  
Author(s):  
Junko Suzuki ◽  
Yunn-Yi Chen ◽  
Gary K. Scott ◽  
Sandy DeVries ◽  
Koei Chin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Histone Deacetylase ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Protein Acetylation ◽  
Malignant Breast

scholarly journals Expression of Annexin A2 Promotes Cancer Progression in Estrogen Receptor Negative Breast Cancers

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1582 ◽  
Author(s):  
Amira F. Mahdi ◽  
Beatrice Malacrida ◽  
Joanne Nolan ◽  
Mary E. McCumiskey ◽  
Anne B. Merrigan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cell Lines ◽  
Cancer Progression ◽  
Annexin A2 ◽  
Breast Cancer Progression ◽  
Migration And Invasion ◽  
Breast Cancer Cell Lines ◽  
Cancer Subtypes ◽  
Estrogen Receptor Negative

When breast cancer progresses to a metastatic stage, survival rates decline rapidly and it is considered incurable. Thus, deciphering the critical mechanisms of metastasis is of vital importance to develop new treatment options. We hypothesize that studying the proteins that are newly synthesized during the metastatic processes of migration and invasion will greatly enhance our understanding of breast cancer progression. We conducted a mass spectrometry screen following bioorthogonal noncanonical amino acid tagging to elucidate changes in the nascent proteome that occur during epidermal growth factor stimulation in migrating and invading cells. Annexin A2 was identified in this screen and subsequent examination of breast cancer cell lines revealed that Annexin A2 is specifically upregulated in estrogen receptor negative (ER-) cell lines. Furthermore, siRNA knockdown showed that Annexin A2 expression promotes the proliferation, wound healing and directional migration of breast cancer cells. In patients, Annexin A2 expression is increased in ER- breast cancer subtypes. Additionally, high Annexin A2 expression confers a higher probability of distant metastasis specifically for ER- patients. This work establishes a pivotal role of Annexin A2 in breast cancer progression and identifies Annexin A2 as a potential therapeutic target for the more aggressive and harder to treat ER- subtype.

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