Anti-estrogenic actions of histone deacetylase inhibitors in MCF-7 breast cancer cells.

@article{DeLosSantos2007AntiestrogenicAO,
  title={Anti-estrogenic actions of histone deacetylase inhibitors in MCF-7 breast cancer cells.},
  author={Maxy B. De Los Santos and Olaia A Mart{\'i}nez-Iglesias and Ana Aranda},
  journal={Endocrine-related cancer},
  year={2007},
  volume={14 4},
  pages={
          1021-8
        }
}
Anti-estrogens are the current endocrine therapy of choice in the treatment of estrogen receptor (ER)-positive breast cancers. Histone deacetylase inhibitors (HDACi) also constitute a promising treatment for therapy, and combination of anti-estrogens with HDACi may improve efficacy while reducing side effects. We have examined the effect of the HDACi sodium butyrate and suberoylanilide hydroxamic acid (SAHA), alone and in combination with 17beta-estradiol (E2) and the pure anti-estrogen ICI 182… 

Figures from this paper

A Chimeric SERM–Histone Deacetylase Inhibitor Approach to Breast Cancer Therapy
TLDR
A superior hybrid caused significant cell death in ER (−) human breast cancer cells and elicited cell death at the same concentration as the parent SERM in combination treatment and at an earlier time point.
Efficacy of the dietary histone deacetylase inhibitor butyrate alone or in combination with vitamin A against proliferation of MCF-7 human breast cancer cells
  • F. O. Andrade, M. Nagamine, +8 authors T. P. Ong
  • Biology, Chemistry
    Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
  • 2012
TLDR
The data show that RARβ may represent a molecular target for butyrate in breast cancer cells, and its effectiveness as a dietary HDACi should be considered for use in combinatorial strategies with more active retinoids, especially in breast cancers in which RAR β is epigenetically altered.
Manipulating Protein Acetylation in Breast Cancer: A Promising Approach in Combination with Hormonal Therapies?
TLDR
Different aspects of HDACs will be described and underline the clinical interest of HDIs in the context of breast cancer resistance to hormone therapies (HTs) in combination with hormonal therapies.
The histone deacetylase inhibitor suberoylanilide hydroxamic acid induces growth inhibition and enhances taxol-induced cell death in breast cancer
TLDR
SAHA increased the anti-tumor effects of taxol in breast cancer in vitro and in vivo and the combination of SAHA and taxol may have therapeutic potential in the treatment of breast cancer.
Activation of the unliganded estrogen receptor by prolactin in breast cancer cells
TLDR
It is shown that PRL is able to activate the unliganded estrogen receptor (ER) and ligand-independent ERα activation appears to be an important component of the proliferative and transcriptional actions of PRL in breast cancer cells.
Studies on the role of two proteins in breast cancer - histone deacetylase 11 in estrogen receptor positive breast cancer and the redox protein memo in metastasis and tumorigenesis
TLDR
The finding that HDAC11 has oncogenic potential in ER-positive breast cancer and therefore might be a new target for therapy is shown, and Memo has prognostic value for patients who received endocrine therapy.
The histone deacetylase inhibitor Suberoylanilide Hydroxamic Acid (SAHA) as a therapeutic agent in rhabdomyosarcoma
TLDR
While SAHA is effective against ERMS and ARMS tumor cells in vitro, it has divergent in vivo effects, and data suggest SAHA as a possible therapeutic agent for clinical testing in patients with fusion protein-positive RMS.
...
1
2
3
4
...

References

SHOWING 1-10 OF 55 REFERENCES
Histone deacetylase inhibition and estrogen receptor alpha levels modulate the transcriptional activity of partial antiestrogens.
TLDR
In conclusion, inhibition of HDAC enzymatic activity and modulation of ERalpha levels tightly control the relative agonist activity of partial antiestrogens on a stably integrated reporter transgene.
Combined effects of retinoic acid and histone deacetylase inhibitors on human neuroblastoma SH-SY5Y cells
TLDR
The results show the strong antitumorigenic effects of HDACi in neuroblastoma cells and reinforce the idea that combination therapy could be useful to inhibit tumor growth.
The histone deacetylase inhibitor suberoylanilide hydroxamic acid induces differentiation of human breast cancer cells.
TLDR
It is proposed that SAHA has profound antiproliferative activity by causing these cells to undergo cell cycle arrest and differentiation that is dependent on the presence of SAHA.
Histone Deacetylase Inhibitor Trichostatin A Represses Estrogen Receptor α-Dependent Transcription and Promotes Proteasomal Degradation of Cyclin D1 in Human Breast Carcinoma Cell Lines
TLDR
It is shown that tamoxifen effectively induces cyclin D1 down-regulation through both ER α-dependent and ERα-independent mechanisms, providing an important new strategy for combating resistance to antiestrogens.
Histone Deacetylase Inhibitor Trichostatin A Represses Estrogen Receptor-Dependent Transcription and Promotes Proteasomal Degradation of Cyclin D 1 in Human Breast Carcinoma Cell Lines
TLDR
The data show that TSA effectively induces cyclin D1 down-regulation through both ER -dependent and ER -independent mechanisms, providing an important new strategy for combating resistance to antiestrogens.
Histone deacetylase inhibitor trichostatin A represses estrogen receptor alpha-dependent transcription and promotes proteasomal degradation of cyclin D1 in human breast carcinoma cell lines.
  • J. Alao, E. Lam, +7 authors D. Vigushin
  • Biology
    Clinical cancer research : an official journal of the American Association for Cancer Research
  • 2004
TLDR
Taken together, the data show that TSA effectively induces cyclin D1 down-regulation through both ERalpha-dependent and ER alpha-independent mechanisms, providing an important new strategy for combating resistance to antiestrogens.
A Pure Estrogen Antagonist Inhibits Cyclin E-Cdk2 Activity in MCF-7 Breast Cancer Cells and Induces Accumulation of p130-E2F4 Complexes Characteristic of Quiescence*
TLDR
Treatment of MCF-7 breast cancer cells with the pure estrogen antagonist ICI 182780 results in inhibition of cyclin E-Cdk2 activity prior to a decrease in the G1 to S phase transition, resulting in the arrest of MCf-7 cells in a state with characteristics of quiescence (G0), as opposed to G1 arrest.
Down-regulation of p21WAF1/CIP1 or p27Kip1 abrogates antiestrogen-mediated cell cycle arrest in human breast cancer cells.
TLDR
It is demonstrated that depletion of either p21 or p27 can mimic estrogen-stimulated cell cycle activation and indicate that both of these KIPs are critical mediators of the therapeutic effects of antiestrogens in breast cancer.
Down-regulation of p 21 WAF 1 y CIP 1 or p 27 Kip 1 abrogates antiestrogen-mediated cell cycle arrest in human breast cancer cells
TLDR
It is demonstrated that depletion of either p21 or p27 can mimic estrogen-stimulated cell cycle activation and indicate that both of these KIPs are critical mediators of the therapeutic effects of antiestrogens in breast cancer.
Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer
TLDR
Investigating aspects of HDACi action both in vitro and in vivo will further improve the design of optimized clinical protocols and help to understand the role of histone deacetylases in tumorigenesis.
...
1
2
3
4
5
...