p53-independent upregulation of p21 super(WAF1) in NIH 3T3 cells malignantly transformed by mot-2

Mot-2 protein is shown to interact with p53 and inhibit its transcriptional activation function. Mot-2 overexpressing stable clones of NIH 3T3 cells were malignantly transformed, however, they had a high level of expression of a p53 downstream gene, p21 super(WAF1). The present study was undertaken to elucidate possible molecular mechanism(s) of such upregulation. An increased level of p21 super(WAF1) expression was detected in stable transfectants although an exogenous reporter gene driven by p21 super(WAF1) promoter exhibited lower activity in these cells suggesting that some post-transcriptional mechanism contributes to upregulation. Western analyses of transient and stable clones revealed that upregulation of p21 super(WAF1) in stable NIH 3T3/mot-2 cells may be mediated by cyclin D1 and cdk-2.