MN/CA IX (MN) exhibits a strong association with tumours. Co-transfection experiments revealed that in MaTu cells the activity of the (-173;+31) MN promoter construct was repressed by the wild type p53 in a dose-responsive manner and stimulated by the (143(Val-->Ala)) mutant. Upregulation of endogenous p53 by mitomycin C treatment in MaTu cells also had a profound effect on MN expression as well as the activity of MN promoter in a reporter construct. p53 can thus modulate MN expression and at least in a subset of tumours the changed p53 status might be responsible for MN positivity. Co-transfections with internally deleted MN promoter constructs demonstrated that the wild type p53 exerts its repression activity on the level of the basal transcriptional machinery and not on a particular cis element within the MN promoter.