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Emerging evidence has demonstrated that upregulated expression of  KIAA1199  in human cancer bodes for poor survival. The regulatory mechanism controlling  KIAA1199  expression in cancer remains to be characterized. In the present study, we have isolated and characterized the human  KIAA1199  promoter in terms of regulation of  KIAA1199  gene expression. A 3.3 kb fragment of human genomic DNA containing the 5′-flanking sequence of the  KIAA1199  gene possesses both suppressive and activating elements. Employing a deletion mutagenesis approach, a 1.4 kb proximal region was defined as the basic  KIAA1199  promoter containing a TATA-box close to the transcription start site. A combination of 5′-primer extension study with 5′RACE DNA sequencing analysis revealed one major transcription start site that is utilized in the human  KIAA1199  gene. Bioinformatics analysis suggested that the 1.4 kb  KIAA1199  promoter contains putative activating regulatory elements, including activator protein-1(AP-1), Twist-1, and NF-κB sites. Sequential deletion and site-direct mutagenesis analysis demonstrated that the AP-1 and distal NF-κB sites are required for  KIAA1199  gene expression. Further analyses using an electrophoretic mobility-shift assay and chromatin immunoprecipitation confirmed the requirement of these  cis - and  trans -acting elements in controlling  KIAA1199  gene expression. Finally, we found that upregulated  KIAA1199  expression in human breast cancer specimens correlated with hypomethylation of the regulatory region. Involvement of DNA methylation in regulation of  KIAA1199  expression was recapitulated in human breast cancer cell lines. Taken together, our study unraveled the regulatory mechanisms controlling  KIAA1199  gene expression in human cancer.

Transcriptional and Epigenetic Regulation of KIAA1199 Gene Expression in Human Breast Cancer