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http://purl.uniprot.org/citations/17545584http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17545584http://www.w3.org/2000/01/rdf-schema#comment"The Bmi-1 oncogene is overexpressed in a number of malignancies including breast cancer. In addition to Bmi-1, mammalian cells also express four other polycomb group (PcG) proteins that are closely related to Bmi-1. Virtually nothing is known about the role of these PcG proteins in oncogenesis. We have recently reported that Mel-18, a Bmi-1-related PcG protein, negatively regulates Bmi-1 expression, and that its expression negatively correlates with Bmi-1 in proliferating and senescing human fibroblasts. Here, we report that the expression of Bmi-1 and Mel-18 inversely correlates in a number of breast cancer cell lines and in a significant number of breast tumor samples. Overexpression of Mel-18 results in repression of Bmi-1 and reduction of the transformed phenotype in malignant breast cancer cells. Furthermore, the repression of Bmi-1 by Mel-18 is accompanied by the reduction of Akt/protein kinase B (PKB) activity in breast cancer cells. Similarly, Bmi-1 knockdown using RNA interference approach results in down-regulation of Akt/PKB activity and reduction in transformed phenotype of MCF7 cells. Importantly, we show that overexpression of constitutively active Akt overrides tumor-suppressive effect of Mel-18 overexpression and the knockdown of Bmi-1 expression. Thus, our studies suggest that Mel-18 and Bmi-1 may regulate the Akt pathway in breast cancer cells, and that Mel-18 functions as a tumor suppressor by repressing the expression of Bmi-1 and consequently down-regulating Akt activity."xsd:string
http://purl.uniprot.org/citations/17545584http://purl.org/dc/terms/identifier"doi:10.1158/0008-5472.can-06-4368"xsd:string
http://purl.uniprot.org/citations/17545584http://purl.uniprot.org/core/author"Zeng M.S."xsd:string
http://purl.uniprot.org/citations/17545584http://purl.uniprot.org/core/author"Guo B.H."xsd:string
http://purl.uniprot.org/citations/17545584http://purl.uniprot.org/core/author"Yadav A."xsd:string
http://purl.uniprot.org/citations/17545584http://purl.uniprot.org/core/author"Guo W.J."xsd:string
http://purl.uniprot.org/citations/17545584http://purl.uniprot.org/core/author"Band V."xsd:string
http://purl.uniprot.org/citations/17545584http://purl.uniprot.org/core/author"Dimri G.P."xsd:string
http://purl.uniprot.org/citations/17545584http://purl.uniprot.org/core/author"Song L.B."xsd:string
http://purl.uniprot.org/citations/17545584http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17545584http://purl.uniprot.org/core/name"Cancer Res"xsd:string
http://purl.uniprot.org/citations/17545584http://purl.uniprot.org/core/pages"5083-5089"xsd:string
http://purl.uniprot.org/citations/17545584http://purl.uniprot.org/core/title"Mel-18 acts as a tumor suppressor by repressing Bmi-1 expression and down-regulating Akt activity in breast cancer cells."xsd:string
http://purl.uniprot.org/citations/17545584http://purl.uniprot.org/core/volume"67"xsd:string
http://purl.uniprot.org/citations/17545584http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17545584
http://purl.uniprot.org/citations/17545584http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17545584
http://purl.uniprot.org/uniprot/#_J3KT13-mappedCitation-17545584http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17545584
http://purl.uniprot.org/uniprot/#_P35226-mappedCitation-17545584http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17545584
http://purl.uniprot.org/uniprot/#_P35227-mappedCitation-17545584http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17545584
http://purl.uniprot.org/uniprot/#_Q5U0M5-mappedCitation-17545584http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17545584
http://purl.uniprot.org/uniprot/#_Q6IB93-mappedCitation-17545584http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17545584
http://purl.uniprot.org/uniprot/P35226http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17545584
http://purl.uniprot.org/uniprot/Q6IB93http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17545584
http://purl.uniprot.org/uniprot/J3KT13http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17545584