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rdf:type |
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lifeskim:mentions |
umls-concept:C0018270,
umls-concept:C0039286,
umls-concept:C0044602,
umls-concept:C0109317,
umls-concept:C0140080,
umls-concept:C0164786,
umls-concept:C0285761,
umls-concept:C0332291,
umls-concept:C0376515,
umls-concept:C0441889,
umls-concept:C0442805,
umls-concept:C0665341,
umls-concept:C0678222,
umls-concept:C0752312,
umls-concept:C0812228,
umls-concept:C1123005,
umls-concept:C1150481,
umls-concept:C1150579,
umls-concept:C1333340,
umls-concept:C1366882,
umls-concept:C1368105,
umls-concept:C1370600,
umls-concept:C1451005,
umls-concept:C1518174,
umls-concept:C1704259,
umls-concept:C1705325,
umls-concept:C1705767,
umls-concept:C1705791,
umls-concept:C1705987,
umls-concept:C1709059
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pubmed:issue |
3
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pubmed:dateCreated |
2009-11-10
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pubmed:abstractText |
We recently showed that estrogen withdrawal from the ERalpha(+), high Bcl-2-expressing breast carcinoma cells (MCF-7B) reduced Bcl-2 protein levels while increasing cell-cell adhesion, and junction formation. Here we compared these cells with the ERalpha(+) and low Bcl-2-expressing MCF-7 cells and with the normal mammary epithelial cell line MCF-10-2A not expressing ERalpha or Bcl-2. All cell lines expressed normal HER2. Antiestrogen (Tamoxifen and ICI 182,780) treatment increased Bcl-2 levels in both MCF-7 and -7B cells and led to the formation of acinar structures. This treatment led to the dissociation of junctions and redistribution of junctional components to the cytoplasm in MCF-10-2A and -7 cells, while in MCF-7B cells junctional proteins redistributed to membranes. Antiestrogen treatment decreased PI3K/Akt activation and increased ERK activation regardless of ERalpha status. IGF-1R was inactivated in the antiestrogen-treated MCF-7 cells while it was activated in MCF-7B cells. Our data show that Tamoxifen and ICI 182,780 can induce growth inhibitory effects via the sustained activation/inactivation of signaling pathways that regulate cell survival, cell death and differentiation in the absence of ERalpha. Furthermore, Bcl-2 overexpression may alter the functional interactions among these pathways in response to antiestrogens, which also may provide a potential explanation for the observation that Bcl-2 overexpressing tumors have a better prognosis.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Connexins,
http://linkedlifedata.com/resource/pubmed/chemical/Estradiol,
http://linkedlifedata.com/resource/pubmed/chemical/Estrogen Receptor alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Extracellular Signal-Regulated MAP...,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, IGF Type 1,
http://linkedlifedata.com/resource/pubmed/chemical/Selective Estrogen Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Tamoxifen,
http://linkedlifedata.com/resource/pubmed/chemical/fulvestrant
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1573-7217
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
118
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
605-21
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:19002577-Blotting, Western,
pubmed-meshheading:19002577-Breast Neoplasms,
pubmed-meshheading:19002577-Cell Adhesion,
pubmed-meshheading:19002577-Cell Line, Tumor,
pubmed-meshheading:19002577-Cell Movement,
pubmed-meshheading:19002577-Cell Proliferation,
pubmed-meshheading:19002577-Connexins,
pubmed-meshheading:19002577-Estradiol,
pubmed-meshheading:19002577-Estrogen Receptor alpha,
pubmed-meshheading:19002577-Extracellular Signal-Regulated MAP Kinases,
pubmed-meshheading:19002577-Female,
pubmed-meshheading:19002577-Fluorescent Antibody Technique,
pubmed-meshheading:19002577-Humans,
pubmed-meshheading:19002577-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:19002577-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:19002577-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:19002577-Receptor, IGF Type 1,
pubmed-meshheading:19002577-Selective Estrogen Receptor Modulators,
pubmed-meshheading:19002577-Signal Transduction,
pubmed-meshheading:19002577-Tamoxifen
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pubmed:year |
2009
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pubmed:articleTitle |
Tamoxifen and ICI 182,780 increase Bcl-2 levels and inhibit growth of breast carcinoma cells by modulating PI3K/AKT, ERK and IGF-1R pathways independent of ERalpha.
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pubmed:affiliation |
Department of Cell Biology, University of Alberta, 6-24 Medical Sciences Building, Edmonton, AB, Canada, T6G 2H7.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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