---------- Forwarded message ----------
From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Sat, Jun 28, 2008 at 4:00 PM
Subject: Identification, and functional analysis of Ska2 interaction with the glucocorticoid receptor.
To: mesothelioma77@gmail.com
[1]J Endocrinol. 2008 Jun 26;
Ray D, Rice L, Waters C, Eccles J, Garside H, Sommer P, Kay P, Blackhall F, Zeef L, Telfer B, Stratford I, Clarke R, Singh D, White A, Stevens A
Glucocorticoid receptors (GR) have profound anti-survival effects on human small cell lung cancer (SCLC). To explore the basis of these effects, protein partners for GR were sought using a yeast two-hybrid screen. We discovered a novel gene, FAM33A, subsequently identified as a Ska1 partner and involved in mitosis, and so renamed Ska2. We produced an anti-peptide antibody which specifically recognized full-length, human Ska2 to measure expression in human cell lines, and tissues. There was wide variation in expression across multiple cell lines, but none detected in the liver cell line HepG2. A xenograft model of human SCLC had intense staining and archival tissue revealed Ska2 in several human lung, and breast tumours. Ska2 was found in the cytoplasm, where it co-localised with GR but nuclear expression of Ska 2 was seen in breast tumours. Ska2 overexpression increased glucocorticoid transactivation in HepG2 cells while Ska2 knockdown in A549 human lung epithelial cells decreased transactivation and prevented dexamethasone inhibition of proliferation. Glucocorticoid treatment decreased Ska2 protein levels in A549 cells, as did staurosporin, phorbol ester, and trichostatin A; all agents that inhibit cell proliferation. Overexpression of Ska2, potentiated the proliferative response to IGF-I exposure, and knockdown with shRNA caused cells to arrest in mitosis. Ska2 has recently been identified in HeLa S3 cells as part of a complex which is critical for spindle checkpoint silencing and exit from mitosis. Our new data show involvement in cell proliferation and glucocorticoid signaling; with implications for understanding how glucocorticoids impact on cell fate.
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Source: http://www.hubmed.org/display.cgi?uids=18583474
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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Sat, Jun 28, 2008 at 4:00 PM
Subject: Identification, and functional analysis of Ska2 interaction with the glucocorticoid receptor.
To: mesothelioma77@gmail.com
[1]J Endocrinol. 2008 Jun 26;
Ray D, Rice L, Waters C, Eccles J, Garside H, Sommer P, Kay P, Blackhall F, Zeef L, Telfer B, Stratford I, Clarke R, Singh D, White A, Stevens A
Glucocorticoid receptors (GR) have profound anti-survival effects on human small cell lung cancer (SCLC). To explore the basis of these effects, protein partners for GR were sought using a yeast two-hybrid screen. We discovered a novel gene, FAM33A, subsequently identified as a Ska1 partner and involved in mitosis, and so renamed Ska2. We produced an anti-peptide antibody which specifically recognized full-length, human Ska2 to measure expression in human cell lines, and tissues. There was wide variation in expression across multiple cell lines, but none detected in the liver cell line HepG2. A xenograft model of human SCLC had intense staining and archival tissue revealed Ska2 in several human lung, and breast tumours. Ska2 was found in the cytoplasm, where it co-localised with GR but nuclear expression of Ska 2 was seen in breast tumours. Ska2 overexpression increased glucocorticoid transactivation in HepG2 cells while Ska2 knockdown in A549 human lung epithelial cells decreased transactivation and prevented dexamethasone inhibition of proliferation. Glucocorticoid treatment decreased Ska2 protein levels in A549 cells, as did staurosporin, phorbol ester, and trichostatin A; all agents that inhibit cell proliferation. Overexpression of Ska2, potentiated the proliferative response to IGF-I exposure, and knockdown with shRNA caused cells to arrest in mitosis. Ska2 has recently been identified in HeLa S3 cells as part of a complex which is critical for spindle checkpoint silencing and exit from mitosis. Our new data show involvement in cell proliferation and glucocorticoid signaling; with implications for understanding how glucocorticoids impact on cell fate.
___
Source: http://www.hubmed.org/display.cgi?uids=18583474
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~
Powered by [5]RssFwd, a service of [6]Blue Sky Factory, Inc