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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Fri, Aug 1, 2008 at 4:32 PM
Subject: Changes in subcellular localisation of MI-ER1alpha, a novel oestrogen receptor-alpha interacting protein, is associated with breast cancer progression.
To: mesothelioma77@gmail.com
[1]Br J Cancer. 2008 Jul 29;
McCarthy PL, Mercer FC, Savicky MW, Carter BA, Paterno GD, Gillespie LL
The oestrogen receptor-alpha (ERalpha) plays a key role in breast development and tumorigenesis and inhibiting its activity remains a prime strategy in the treatment of ERalpha-positive breast cancers. Thus, elucidation of the molecular mechanisms responsible for regulating ERalpha activity may facilitate the design of new, more effective breast cancer therapies. The MI-ER1alpha is a novel transcriptional repressor that contains an LXXLL motif for interaction with nuclear hormone receptors. We investigated the ability of MI-ER1alpha to bind to ERalpha in HEK293 and MCF-7 breast carcinoma cells, using co-immunoprecipitation assays. In both cell lines, MI-ER1alpha interacted with ERalpha in the presence and absence of oestrogen, but the interaction was stronger in the absence of ligand. Functional analysis revealed that overexpression of MI-ER1alpha in T47D breast carcinoma cells results in inhibition of oestrogen-stimulated anchorage-independent growth, suggesting that MI-ER1alpha may play a role in regulating breast carcinoma cell proliferation in vivo. To explore this further, we performed an immunohistochemical analysis of normal breast tissue and breast carcinoma; a total of 110 cases were examined in whole tissue sections and 771 cases were analysed in tissue microarrays. No consistent difference in the MI-ER1alpha expression level between normal breast tissue and breast carcinoma was discernible. However, there was a dramatic shift in the subcellular localisation: nuclear MI-ER1alpha was detectable in 75% of normal breast samples and in 77% of hyperplasia, but in breast carcinoma, only 51% of DCIS, 25% of ILC and 4% of IDC contained nuclear staining. This shift from nuclear to cytoplasmic localisation of MI-ER1alpha during breast cancer progression suggests that loss of nuclear MI-ER1alpha might contribute to the development of invasive breast carcinoma.British Journal of Cancer advance online publication, 29 July 2008; doi:10.1038/sj.bjc.6604518 www.bjcancer.com.
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Source: http://www.hubmed.org/display.cgi?uids=18665173
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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Fri, Aug 1, 2008 at 4:32 PM
Subject: Changes in subcellular localisation of MI-ER1alpha, a novel oestrogen receptor-alpha interacting protein, is associated with breast cancer progression.
To: mesothelioma77@gmail.com
[1]Br J Cancer. 2008 Jul 29;
McCarthy PL, Mercer FC, Savicky MW, Carter BA, Paterno GD, Gillespie LL
The oestrogen receptor-alpha (ERalpha) plays a key role in breast development and tumorigenesis and inhibiting its activity remains a prime strategy in the treatment of ERalpha-positive breast cancers. Thus, elucidation of the molecular mechanisms responsible for regulating ERalpha activity may facilitate the design of new, more effective breast cancer therapies. The MI-ER1alpha is a novel transcriptional repressor that contains an LXXLL motif for interaction with nuclear hormone receptors. We investigated the ability of MI-ER1alpha to bind to ERalpha in HEK293 and MCF-7 breast carcinoma cells, using co-immunoprecipitation assays. In both cell lines, MI-ER1alpha interacted with ERalpha in the presence and absence of oestrogen, but the interaction was stronger in the absence of ligand. Functional analysis revealed that overexpression of MI-ER1alpha in T47D breast carcinoma cells results in inhibition of oestrogen-stimulated anchorage-independent growth, suggesting that MI-ER1alpha may play a role in regulating breast carcinoma cell proliferation in vivo. To explore this further, we performed an immunohistochemical analysis of normal breast tissue and breast carcinoma; a total of 110 cases were examined in whole tissue sections and 771 cases were analysed in tissue microarrays. No consistent difference in the MI-ER1alpha expression level between normal breast tissue and breast carcinoma was discernible. However, there was a dramatic shift in the subcellular localisation: nuclear MI-ER1alpha was detectable in 75% of normal breast samples and in 77% of hyperplasia, but in breast carcinoma, only 51% of DCIS, 25% of ILC and 4% of IDC contained nuclear staining. This shift from nuclear to cytoplasmic localisation of MI-ER1alpha during breast cancer progression suggests that loss of nuclear MI-ER1alpha might contribute to the development of invasive breast carcinoma.British Journal of Cancer advance online publication, 29 July 2008; doi:10.1038/sj.bjc.6604518 www.bjcancer.com.
___
Source: http://www.hubmed.org/display.cgi?uids=18665173
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