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Caliban, the Drosophila ortholog of human Nuclear export mediator factor (NEMF), is a recently identified regulator of the intrinsic apoptotic signaling pathway in response to DNA damage; however, the mechanism governing its expression after DNA damage remains unclear. In this study, we demonstrated that DNA damage upregulated caliban expression concomitant with p53 activation. Over-expression of p53 upregulated the mRNA and protein levels of caliban. We characterized the core region of the caliban promoter, which exhibited enhanced activity following DNA damage or p53 activation. Further analysis of the caliban promoter revealed a p53-binding site that directly interacts with p53 in response to DNA damage. Moreover, mutation of this p53-binding site or knock-down of p53 expression abolished the DNA damage-induced increase in caliban promoter activity, confirming p53’s critical role in regulating caliban expression. Taken together, our findings indicate that caliban is a direct transcriptional target of p53 in response to DNA damage.