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Identification of ANKRD11 As a P53 Coactivator

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Identification of ANKRD11 As a P53 Coactivator Research Article 3541 Identification of ANKRD11 as a p53 coactivator Paul M. Neilsen1,*, Kelly M. Cheney1, Chia-Wei Li2, J. Don Chen2, Jacqueline E. Cawrse1, Renée B. Schulz1, Jason A. Powell3, Raman Kumar1 and David F. Callen1 1Breast Cancer Genetics Group, Dame Roma Mitchell Cancer Research Laboratories, Discipline of Medicine, University of Adelaide and Hanson Institute, IMVS, Adelaide, SA 5000, Australia 2Department of Pharmacology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, NJ 08854-5635, USA 3Cytokine Receptor Laboratory, Department of Human Immunology, Hanson Institute, IMVS, Adelaide, SA 5000, Australia *Author for correspondence (e-mail: [email protected]) Accepted 29 July 2008 Journal of Cell Science 121, 3541-3552 Published by The Company of Biologists 2008 doi:10.1242/jcs.026351 Summary The ability of p53 to act as a transcription factor is critical for ANKRD11 enhanced the DNA-binding properties of mutant its function as a tumor suppressor. Ankyrin repeat domain 11, p53R273H to the CDKN1A promoter, suggesting that ANKRD11 ANKRD11 (also known as ANR11 or ANCO1), was found to can mediate the restoration of normal p53 function in some be a novel p53-interacting protein that enhanced the cancer-related p53 mutations. In addition, ANKRD11 itself was transcriptional activity of p53. ANKRD11 expression was shown found to be a novel p53 target gene. These findings demonstrate to be downregulated in breast cancer cell lines. Restoration of a role for ANKRD11 as a p53 coactivator and suggest the ANKRD11 expression in MCF-7 (wild-type p53) and MDA-MB- involvement of ANKRD11 in a regulatory feedback loop with 468 (p53R273H mutant) cells suppressed their proliferative and p53. clonogenic properties through enhancement of CDKN1A (p21waf1/CIP1) expression. ShRNA-mediated silencing of ANKRD11 expression reduced the ability of p53 to activate Supplementary material available online at CDKN1A expression. ANKRD11 was shown to associate with http://jcs.biologists.org/cgi/content/full/121/21/3541/DC1 the p53 acetyltransferases and cofactors, P/CAF and hADA3. Exogenous ANKRD11 expression enhanced the levels of Key words: Acetylation, Ankyrin repeat domain protein, Breast acetylated p53 in both MCF-7 and MDA-MB-468 cells. cancer, p53, p53 mutant rescue Introduction proven to be a challenging task because of the complex Journal of Cell Science The p53 protein is the most important tumor suppressor in the cell biomechanistics that occur during the restoration of mutant p53 and is described as ‘the guardian of the genome’ (Lane, 1992). The function. function of p53 is predominantly dependent on its activity as a The p53 transcription factor is stabilized and activated in response sequence-specific transcription factor, controlling the expression of to various forms of intracellular or extracellular stress. Stabilization various target genes that mediate biological functions such as cell- and activation of p53 occurs through a complex pattern of post- cycle arrest, apoptosis, senescence, differentiation, DNA repair and translational modifications, including phosphorylation and inhibition of angiogenesis and metastasis (Liu and Chen, 2006). acetylation. The acetylation of specific lysine residues of p53 is Approximately 50% of all cancers contain a mutation in the TP53 mediated by several acetyltransferases, including p300/CBP gene (Vogelstein et al., 2000). The six most frequently occurring (Lys164, Lys370, Lys372, Lys373, Lys381, Lys382 and Lys386), tumorigenic mutations of p53 cluster within the DNA-binding Tip60/hMOF (Lys120) and P/CAF (Lys320) (Gu and Roeder, 1997; surface, involving residues that either directly contact DNA (‘DNA- Sakaguchi et al., 1998; Sykes et al., 2006; Tang et al., 2008). Earlier contact’ mutations – residues R248 and R273) or perturb the studies have shown that acetylation of p53 promotes its ability to structural integrity of the DNA-binding surface of p53 (‘structural’ bind its cognate DNA-response element in vitro (Gu and Roeder, mutations – residues R175, G245, R249 and R282) (Bullock and 1997; Sakaguchi et al., 1998); however, these findings are not Fersht, 2001). DNA-contact mutants generally retain a similar consistent with recent in vivo data (Liu and Chen, 2006; Tang et structural integrity and thermodynamic stability to that displayed al., 2008; Toledo and Wahl, 2006). It has since been shown that the by wild-type p53; however, the mutation might significantly impair critical function of acetylation in vivo is not to enhance the DNA- or even completely abrogate its ability to interact with its cognate binding affinity of p53, but rather to enhance its interaction with DNA-response element (Bullock et al., 2000). Rescue of DNA- coactivators or histone acetyltransferases (HATs) (Barlev et al., contact mutants has been demonstrated through restoration of their 2001), or perturb its interaction with Mdm2 (Tang et al., 2008) at DNA-binding affinities following treatment with a p53-derived C- the promoters of p53-responsive genes. Recent evidence also terminal peptide (Selivanova et al., 1997), small p53-activating suggests that acetylation of specific lysine residues in p53 may molecules (CP-257042, CP-31398 and PRIMA-1) (Bykov et al., influence the selection of specific p53 target genes, resulting in 2002; Foster et al., 1999) or the introduction of second site induction of either growth arrest or apoptotic pathways (Di Stefano suppressor mutations (Brachmann et al., 1998). Despite these recent et al., 2005). hADA3 (alteration/deficiency in activation) has been advances, the development of successful pharmacological identified as a novel p53-interacting protein capable of recruiting therapeutics designed to rescue p53 DNA-contact mutants has p300/CBP and P/CAF to p53 (Wang et al., 2001). Ectopic expression 3542 Journal of Cell Science 121 (21) of hADA3 increased the stability and transcriptional activity of p53, ANKRD11-myc and GFP-p14ARF were ectopically expressed in and was shown to have an essential role in p53 acetylation (Wang HEK293T cells and imaged using confocal microscopy (Fig. 1C). et al., 2001). Nevertheless, we currently do not have a Coimmunolocalization results showed that ANKRD11-myc comprehensive understanding of the complex molecular localized exclusively to extranucleolar p14ARF foci (filled mechanisms involved in the regulation of p53 acetylation. arrowheads), but not to the larger nucleolar p14ARF foci (open ANKRD11 was initially selected as a candidate breast cancer arrowheads). Endogenous PML counterstaining showed that PML tumor suppressor gene because of its location within the 16q24.3 bodies were also recruited to ANKRD11/p14ARF-positive breast cancer LOH (loss of heterozygosity) region (Powell et al., extranucleolar inclusions (Fig. 1D) as previously reported (Kashuba 2002). LOH of human chromosome 16q occurs in at least half of et al., 2003). In the absence of exogenous p14ARF, ANKRD11 all breast tumors (Miller et al., 2003) and cytogenetic studies have nuclear foci were observed to exhibit only partial colocalization implicated this to be an early event in breast carcinogenesis (Gong with PML bodies during late G2 phase of the cell cycle (data not et al., 2001). ANKRD11 (also termed ANCO1; official protein shown). This observation suggests that the association of symbol ANR11) was also reported to interact with and suppress ANKRD11-PML complex is enhanced in the presence of p14ARF. the function of the p160 coactivator family, including the oncogene The location of nucleoli in these cells was determined through AIB1 (amplified in breast cancer-1) (Zhang et al., 2004). AIB1 detection of nucleophosmin, and nuclei were counterstained with enhances ligand-dependent transactivation of steroid nuclear DAPI. Further studies were undertaken using glycerol gradient receptors, including estrogen receptor (ER), and is frequently centrifugation of lysates of MCF-7 cells stably expressing GFP- amplified and overexpressed in breast and ovarian cancers (Anzick ANKRD11-myc. Both p53 and PML cofractionated with et al., 1997). ANKRD11 was reported to recruit histone deacetylases ANKRD11-myc (supplementary material Fig. S2), providing (HDACs) through its C-terminus to the AIB1/nuclear receptor preliminary evidence that these proteins may coexist as a complex. complex, resulting in the inhibition of ligand-dependent Detection of p14ARF in these fractions was not possible because the transactivation (Zhang et al., 2004). Based on these findings, we MCF-7 cell line does not express endogenous p14ARF as a result investigated whether ANKRD11 has properties similar to that of a of deletion of the CDKN2A locus (Stott et al., 1998). breast cancer tumor suppressor. In this study we report the functional characterization of ANKRD11 interacts with p53 in vivo and in vitro through the ANKRD11 as a novel p53-interacting protein. We find that ankyrin repeat domain ANKRD11 increases the acetylation of p53, potentiating the DNA- Coimmunoprecipitation experiments were used to determine binding property and transcriptional activity of p53. Findings from whether ANKRD11 interacts with p53 in vivo. Endogenous p53 this study suggest that ANKRD11 might have a crucial role in p53- was detected in protein complexes immunoprecipitated using an mediated tumor suppression and might also be implicated in the anti-ANKRD11 antibody from protein lysates of MCF-7 cells restoration of mutant p53R273H function. We also show that transduced with recombinant
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