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Steroid Receptor Coactivator-1 and Its Family Members Differentially Regulate Transactivation by the Tumor Suppressor Protein p53

Center for Ligand and Transcription (J.W.L, H.-J.K) Hormone Research Center (J.W.L) Department of Biology (S.-K.L) Chonnam National University Kwangju 500–757, Korea
Department of Biochemistry (J.W.K) Paichai University Daejeon 302–735, Korea

The tumor suppressor protein p53 exerts its cell cycle-regulatory effects through its ability to function as a sequence-specific DNA-binding transcription factor. Herein, we show that p53 physically interacts with specific subregions of steroid receptor coactivator-1 (SRC-1) and its family members, p/CIP (p300/CBP interacting protein), xSRC-3, and AIB1 (amplified in breast cancer), originally isolated as transcription coactivators of nuclear receptors, as demonstrated by the yeast and mammalian two-hybrid tests as well as glutathione S-transferase pull-down assays. Interestingly, cotransfection of HeLa cells with SRC-1- or p/CIP expression vector potentiated the p53-mediated transactivation, whereas AIB1 and xSRC-3 were repressive. All of these SRC-1 members, however, similarly stimulated transactivation mediated by nuclear receptors and AP-1, as previously described. These results suggest that SRC-1 and its family members may differentially modulate the p53 transactivation in vivo.

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