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Title[redir]:
Interleukin-6 induces an epithelial–mesenchymal transition phenotype in human breast cancer cells | Oncogene
Description:
Breast tumor interleukin-6 (IL-6) levels increase with tumor grade, and elevated serum IL-6 correlates with poor breast cancer patient survival. Epithelial–mesenchymal transition (EMT) phenotypes such as impaired E-cadherin expression or aberrant Vimentin induction are associated with enhanced metastasis and unfavorable clinical outcome in breast cancer. Despite this fact, few tumor microenvironment-derived extracellular signaling factors capable of provoking such a phenotypic transition have been identified. In this study, we showed that IL-6 promoted E-cadherin repression among a panel of estrogen receptor-α-positive human breast cancer cells. Furthermore, ectopic stable IL-6 expressing MCF-7 breast adenocarcinoma cells (MCF-7IL−6) exhibited an EMT phenotype characterized by impaired E-cadherin expression and induction of Vimentin, N-cadherin, Snail and Twist. MCF-7IL−6 cells formed xenograft tumors that displayed loss of E-cadherin, robust Vimentin induction, increased proliferative indices, advanced tumor grade and undifferentiated histology. Finally, we showed aberrant IL-6 production and STAT3 activation in MCF-7 cells that constitutively express Twist, a metastatic regulator and direct transcriptional repressor of E-cadherin. To our knowledge, this is the first study that shows IL-6 as an inducer of an EMT phenotype in breast cancer cells and implicates its potential to promote breast cancer metastasis.
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Keywords {🔍}
cancer, article, breast, google, scholar, cas, pubmed, cells, interleukin, cell, nature, central, human, tumor, res, epithelialmesenchymal, access, transition, content, metastasis, induces, sasser, ecadherin, cookies, phenotype, sullivan, serum, stat, growth, carcinoma, privacy, oncogene, axel, emt, expression, activation, metastatic, cytokine, research, data, hall, levels, induction, signaling, twist, open, patients, biol, usa, advertising,
Topics {✒️}
nature portfolio permissions reprints privacy policy nature 449 nature research institute advertising ellis io social media author information authors development androgen–estrogen receptors ratio breast tumor microenvironment extra-terminal inhibitor jq1 elicit epithelial–mesenchymal transition cell line-dependent manner author correspondence epithelial–mesenchymal transition phenotype direct transcriptional repressor impaired e-cadherin expression personal data breast cancer cells human breast carcinoma estrogen receptor status murine cancer cells potent growth factor springerlink instant access data protection normal mammary gland permissions mesenchymal stem cells breast cancer patients epithelial-mesenchymal transitions epithelial–mesenchymal transitions metastatic breast cancer epithelial–mesenchymal transition breast cancer biopsies breast cancer relates breast cancer viviana colon carcinoma cells prostate cancer lines metastatic breast carcinoma 3d tumor environments colon carcinoma tumors yang dc ohio state university cell cycle arrest privacy fibroblast secreted factors advanced tumor grade
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headline:Interleukin-6 induces an epithelialâmesenchymal transition phenotype in human breast cancer cells
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datePublished:2009-07-06T00:00:00Z
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headline:Interleukin-6 induces an epithelialâmesenchymal transition phenotype in human breast cancer cells
description:Breast tumor interleukin-6 (IL-6) levels increase with tumor grade, and elevated serum IL-6 correlates with poor breast cancer patient survival. Epithelialâmesenchymal transition (EMT) phenotypes such as impaired E-cadherin expression or aberrant Vimentin induction are associated with enhanced metastasis and unfavorable clinical outcome in breast cancer. Despite this fact, few tumor microenvironment-derived extracellular signaling factors capable of provoking such a phenotypic transition have been identified. In this study, we showed that IL-6 promoted E-cadherin repression among a panel of estrogen receptor-α-positive human breast cancer cells. Furthermore, ectopic stable IL-6 expressing MCF-7 breast adenocarcinoma cells (MCF-7ILâ6) exhibited an EMT phenotype characterized by impaired E-cadherin expression and induction of Vimentin, N-cadherin, Snail and Twist. MCF-7ILâ6 cells formed xenograft tumors that displayed loss of E-cadherin, robust Vimentin induction, increased proliferative indices, advanced tumor grade and undifferentiated histology. Finally, we showed aberrant IL-6 production and STAT3 activation in MCF-7 cells that constitutively express Twist, a metastatic regulator and direct transcriptional repressor of E-cadherin. To our knowledge, this is the first study that shows IL-6 as an inducer of an EMT phenotype in breast cancer cells and implicates its potential to promote breast cancer metastasis.
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