Lithium treatment enhances estradiol-induced proliferation and hyperplasia formation in the uterus of mice

Гунин, А. Г.; Emelianov, Vladimir U.; Mironkin, I. U.; Morozov, M. P.; Tolmachev, Alexei S.

doi:10.1016/j.ejogrb.2003.09.023

Cited by 32 publications

(30 citation statements)

References 35 publications

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“…Using the chromatin immunoprecipitation (ChIP) assay they also identified interactions of ERa and b-catenin antibodies with genes containing TBE and ERE, respectively. These data are consistent with a recent finding, albeit in non-neuronal tissue, that concomitant lithium and estrogen administration to ovariectomized mice results in an increase in estradiol-induced proliferative and morphogenetic changes in the uterus (Gunin et al, 2004).…”

Section: Neurohormone Regulation: Estrogen and Glucocorticoidssupporting

confidence: 82%

Glycogen Synthase Kinase-3: a Putative Molecular Target for Lithium Mimetic Drugs

Gould

Manji

2005

Neuropsychopharmacol

341

253

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Section: Neurohormone Regulation: Estrogen and Glucocorticoidssupporting

confidence: 82%

Glycogen Synthase Kinase-3: a Putative Molecular Target for Lithium Mimetic Drugs

Gould

Manji

2005

Neuropsychopharmacol

341

253

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“…The parallel association between nuclear phospho-b-catenin and ER is in conformity with studies, [24][25][26] that have shown the physical, transcriptional and genetic interaction in vivo between ER and b-catenin on different tissues. However, this is the first study to find a positive correlation between b-catenin and ERb, implying a possible interaction between ERb and b-catenin, similar to the aforementioned interaction between ER and b-catenin.…”

Section: Discussionsupporting

confidence: 59%

Study of phospho-β-catenin subcellular distribution in invasive breast carcinomas in relation to their phenotype and the clinical outcome

et al. 2006

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b-Catenin has a crucial role in cell-cell adhesion as well as a signaling role as a member of the Wnt pathway. The aim of this study was to examine the clinicopathological and prognostic value of phosphorylated b-catenin, as well as its relation to the tumors' phenotype, in breast cancer. Immunohistochemistry was applied on 141 paraffin-embedded breast tissue specimens for the detection of phospho-b-catenin, ER, PR, c-erbB-2, p53, Ki-67, bcl-2, uPAR and TIMP-1. For each case, a phospho-b-catenin index was determined by image analysis. Phospho-b-catenin staining was detected in the cytoplasm and the nucleus of the malignant cells. Cytoplasmic phospho-b-catenin was statistically higher in carcinomas of smaller tumor size (P ¼ 0.030), lower stage (P ¼ 0.026), decreased Ki-67 and high c-erbB-2 immunoreactivity (P ¼ 0.052 and P ¼ 0.037, respectively). Nuclear phospho-b-catenin showed a parallel correlation with ER and ERb (P ¼ 0.022 and P ¼ 0.043, respectively), bcl-2 (P ¼ 0.042), uPAR in cancer cells (P ¼ 0.041) and TIMP-1, although the correlation was borderline (P ¼ 0.066). Cytoplasmic phospho-b-catenin was found to be independently correlated with prolonged disease-free and overall survival (P ¼ 0.046 and P ¼ 0.002, respectively), whereas nuclear localization was correlated with a shortened overall survival (P ¼ 0.046). In conclusion, phospho-b-catenin may have a different involvement in invasive breast carcinomas, according to its subcellular distribution. Nuclear localization seems to be related to an aggressive tumor phenotype, negatively affecting patients' overall survival, whereas cytoplasmic localization is associated with a favorable tumor phenotype and a longer disease-free and overall survival.

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“…In the case of low -catenin concentration, cell-cell interactions are less solid, which provides a foundation for cancer development. It has been reported that the level of -catenin in the uterus was decreased following estrogen action and cancer formation (Fujimoto et al 1998, Nei et al 1999, Miyamoto et al 2000, Gunin et al 2004b. There is a decrease in -catenin expression in uterine epithelia in mice treated with estradiol and histone deacetylase blockers compared with that of mice treated with estradiol alone.…”

Section: Discussionmentioning

confidence: 73%

“…Recent data showed that estrogen also recruits intracellular regulatory systems to bring about its action (Couse & Korach 1999, Deroo et al 2004, Gunin et al 2004b. The scientific literature gives some direct and indirect evidence that the system that maintains the status of histone acetylation interacts with estrogen signalling (Alao et al 2004, Kurtev et al 2004.…”

Section: Introductionmentioning

confidence: 99%

Effects of histone deacetylase inhibitors on estradiol-induced proliferation and hyperplasia formation in the mouse uterus

Гунин¹,

Kapitova²,

Суслонова³

2005

Journal of Endocrinology

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It is suggested that estrogen hormones recruit mechanisms controlling histone acetylation to bring about their effects in the uterus. However, it is not known how the level of histone acetylation affects estrogen-dependent processes in the uterus, especially proliferation and morphogenetic changes. Therefore, this study examined the effects of histone deacetylase blockers, trichostatin A and sodium butyrate, on proliferative and morphogenetic reactions in the uterus under long-term estrogen treatment. Ovariectomized mice were treated with estradiol dipropionate (4 µg per 100 g; s.c., once a week) or vehicle and trichostatin A (0·008 mg per 100 g; s.c., once a day) or sodium butyrate (1% in drinking water), or with no additional treatments for a month. In animals treated with estradiol and trichostatin A or sodium butyrate, uterine mass was increased, and abnormal uterine glands and atypical endometrial hyperplasia were found more often. Both histone deacetylase inhibitors produced an increase in the numbers of mitotic and bromodeoxyuridine-labelled cells in luminal and glandular epithelia, in stromal and myometrial cells. Levels of estrogen receptor-and progesterone receptors in uterine epithelia, stromal and myometrial cells were decreased in mice treated with estradiol and trichostatin A or sodium butyrate. Expression of -catenin in luminal and glandular epithelia was attenuated in mice treated with estradiol with trichostatin A or sodium butyrate. Both histone deacetylase inhibitors have similar unilateral effects; however the action of trichostatin A was more expressed than that of sodium butyrate. Thus, histone deacetylase inhibitors exert proliferative and morphogenetic effects of estradiol. The effects of trichostatin A and sodium butyrate are associated with changes in expression of estrogen receptor-, progesterone receptors and -catenin in the uterus.

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Lithium treatment enhances estradiol-induced proliferation and hyperplasia formation in the uterus of mice

Cited by 32 publications

References 35 publications

Glycogen Synthase Kinase-3: a Putative Molecular Target for Lithium Mimetic Drugs

Glycogen Synthase Kinase-3: a Putative Molecular Target for Lithium Mimetic Drugs

Study of phospho-β-catenin subcellular distribution in invasive breast carcinomas in relation to their phenotype and the clinical outcome

Effects of histone deacetylase inhibitors on estradiol-induced proliferation and hyperplasia formation in the mouse uterus

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