The transporter associated with antigen processing (TAP) I is required for
the major histocompatibility complex (MHC) class I antigen presentation pat
hway, which plays a key role in host tumor surveillance. Since more than 50
% of tumors have a dysfunctional p53, evasion of tumor surveillance by tumo
r cells may be linked to loss of p53 function. Here we found that TAP1 is s
trongly induced by p53 and DNA-damaging agents through a p53-responsive ele
ment. We also found that p73, which is homologous to p53, is capable of ind
ucing TAP1 and cooperates with p53 to activate TAP1. Furthermore, me found
that by inducing TAP1, p53 enhances the transport of MHC class I peptides a
nd expression of surface MHC-peptide complexes, and cooperates with interfe
ron gamma to activate the MHC class I pathway. These results suggest that t
umor surveillance may be a mechanism by which p53 and/or p73 function as tu
mor suppressors.