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Background   NKX3.1  and  PCAN1  are both prostate-specific genes related to prostate development and prostate cancer. So far, little is known about the regulatory mechanisms of the expression of these two genes. In the present study, we found that NKX3.1 upregulated  PCAN1  gene transcription in LNCaP prostate cancer cells. To understand the regulatory mechanisms, our work focused on identifying the functional NKX3.1 binding sites upstream of the  PCAN1  gene, which might be involved in the positive regulation of  PCAN1  expression by NKX3.1.    Results  We cloned and characterized a 2.6 kb fragment upstream of the  PCAN1  gene. Analysis of the 2.6 kb sequence with MatInspector 2.2 revealed five potential binding sites of NKX3.1 transcription factor. Luciferase reporter assays, electrophoretic mobility shift assays, chromatin immunoprecipitation and RNA interference were performed to study the effects of NKX3.1 on  PCAN1  gene expression in prostate cancer cells. Our results showed that  PCAN1  promoter activity and mRNA expression were increased by transfection with the  NKX3.1  containing plasmid (pcDNA3.1- NKX3.1 ) and that  PCAN1  mRNA expression was decreased by RNA interference targeting human  NKX3.1  in LNCaP prostate cancer cells. The results of electrophoretic mobility shift assays and chromatin immunoprecipitation showed that NKX3.1 bound to NBS1 (-1848 to -1836) and NBS3 (-803 to -791) upstream of the  PCAN1  gene. The luciferase reporter assays showed that NBS1 and NBS3 enhanced the promoter activity in pGL 3 -promoter vector with cotransfection of the  NKX3.1  containing plasmid. Furthermore, the deletion of NBS1 or both NBS1 and NBS3 reduced  PCAN1  promoter activity and abolished the positive regulation of  PCAN1  expression by NKX3.1.    Conclusion  Our results suggested that two functional NKX3.1 binding sites located at -1848 to -1836 and -803 to -791 upstream of the  PCAN1  gene were involved in the positive regulation of  PCAN1  gene transcription by NKX3.1.

bmc molecular biology

Characterization of two functional NKX3.1 binding sites upstream of the PCAN1 gene that are involved in the positive regulation of PCAN1 gene transcription