Sp1 and Sp3 transcription factors upregulate the proximal promoter of the human prostate-specific antigen gene in prostate cancer cells

Shin, Toshitaka; Sumiyoshi, Hideaki; Matsuo, Noritaka; Satoh, Fuminori; Nomura, Yoshio; Mimata, Hiromitsu; Yoshioka, Hidekatsu

doi:10.1016/j.abb.2005.01.002

Cited by 21 publications

(21 citation statements)

References 46 publications

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“…These results appear to be consistent with previous studies of relative HDAC4 mRNA levels in different human tissues, which found high levels in the brain, skeletal muscle, heart, and testis (Fischle et al, 1999;Grozinger et al, 1999;Wang et al, 1999). Other investigations have identified roles of Sp1 and other Sp family proteins in driving promoter activity in different human tissues or tissue-specific promoters, including that of neurons, the testis, keratinocytes, the prostate, and the pancreas (McClure et al, 1999;Zhang et al, 1999;Shi et al, 2001;Kaufman et al, 2002;Wilkerson et al, 2002;Naso et al, 2003;Abdelrahim et al, 2004;Tang et al, 2004;Benfante et al, 2005;Shin et al, 2005;Wang and Bannon, 2005). Interestingly, these investigations are supported by our findings of high Sp1 levels in the cortical brain, the testis, the prostate, epidermal skin, and pancreas.…”

Section: Discussionsupporting

confidence: 81%

Regulation of Histone Deacetylase 4 Expression by the SP Family of Transcription Factors

Liu

Pore

Kim

et al. 2006

MBoC

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Histone deacetylases mediate critical cellular functions but relatively little is known about mechanisms controlling their expression, including expression of HDAC4, a class II HDAC implicated in the modulation of cellular differentiation and viability. Endogenous HDAC4 mRNA, protein levels and promoter activity were all readily repressed by mithramycin, suggesting regulation by GC-rich DNA sequences. We validated consensus binding sites for Sp1/Sp3 transcription factors in the HDAC4 promoter through truncation studies and targeted mutagenesis. Specific and functional binding by Sp1/Sp3 at these sites was confirmed with chromatin immunoprecipitation (ChIP) and electromobility shift assays (EMSA). Cotransfection of either Sp1 or Sp3 with a reporter driven by the HDAC4 promoter led to high activities in SL2 insect cells (which lack endogenous Sp1/Sp3). In human cells, restored expression of Sp1 and Sp3 up-regulated HDAC4 protein levels, whereas levels were decreased by RNA-interference-mediated knockdown of either protein. Finally, variable levels of Sp1 were in concordance with that of HDAC4 in a number of human tissues and cancer cell lines. These studies together characterize for the first time the activity of the HDAC4 promoter, through which Sp1 and Sp3 modulates expression of HDAC4 and which may contribute to tissue or cell-line-specific expression of HDAC4. INTRODUCTIONHistone deacetylases (HDACs) all share the ability to deacetylate specific lysines in the tail residues of the core histones, generally resulting in the compaction of chromatin, transcriptional repression, and silencing. There has been an explosion of interest in recent years in the HDACs, because of the panoply of critical cellular functions that have now been linked to HDACs (Grozinger and Schreiber, 2002;Verdin et al., 2003;Sengupta and Seto, 2004;Yang and Gregoire, 2005) .HDACs in general lack DNA binding activity, and appear to mediate their activities as part of large multiprotein complexes (such as the NuRD, Sin3, and CoREST complexes; Hassig et al., 1997;Laherty et al., 1997;Zhang et al., 1997Zhang et al., , 1998, which include non-HDAC proteins and other unique polypeptides that together modulate histone deacetylase activity. An example of the regulation of HDAC activity mediated by protein-protein interactions relates to the SMRT/ N-CoR complex. The silencing mediator of retinoid and thyroid receptor (SMRT) and nuclear receptor corepressor (N-CoR) are nuclear receptor corepressors that bind and enhance the HDAC activity of HDAC3 (Alland et al., 1997;Heinzel et al., 1997;Wen et al., 2000;Guenther et al., 2001;. In contrast to the effects on HDAC3, the deacetylase activity of the class II HDACs (HDAC4, 5, 7, and 9) are not enhanced by binding to the SMRT/N-CoR complex, suggesting that the class II HDACs may recruit enzymatically active HDAC3-SMRT/N-coR complexes for their functional effects (Fischle et al., 2002). Regulation of the expression of class II HDACs may therefore influence the overall function of such multiprotein complexe...

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Section: Discussionsupporting

confidence: 81%

Regulation of Histone Deacetylase 4 Expression by the SP Family of Transcription Factors

Liu

Pore

Kim

et al. 2006

MBoC

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“…Four bands (I, II, III, IV) were detected ( Figure 6a) when protein extracts prepared from RKO cells were incubated with either the consensus element known to bind SP1 as well as SP3 proteins (Shin et al, 2005) Regulation of the cancer-associated DNA polymerase j…”

Section: Polk Transcription Depends On Cre and Sp1 Elementsmentioning

confidence: 99%

Characterization of promoter regulatory elements involved in downexpression of the DNA polymerase κ in colorectal cancer

et al. 2006

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The low-fidelity DNA polymerases thought to be specialized in DNA damage processing are frequently misregulated in cancers. We show here that DNA polymerase kappa (polj), prone to replicate across oxidative and aromatic adducts and known to function in nucleotide excision repair (NER), is downregulated in colorectal tumour biopsies. Contrary to the replicative pold and pola, for which only activating domains were described, we identified an upstream 465-bp-long repressor region in the promoter of POLK. We also found an activating 237-bp region that includes stimulating protein-1 (SP1) and cyclic AMP-responsive element (CRE)-binding sites. Mutations at one CRE-binding site led to a dramatic 80% decrease in promoter activity. Alterations of the SP1-binding site also affected, to a lesser extent, the transcription. Gel shift assays confirmed the role played by CRE/SP1 recognition sequences. Moreover, ectopic expression of SP1 or CRE-binding protein (CREB) protein favoured polj transcription. Finally, we found that polj downexpression in colorectal biopsies correlated with a decreased level of CREB and SP1 transcripts. This work shows that the promoter of POLK is cis-controlled and suggests that silencing of CREB and SP1 proteins could contribute to downregulation of this repair polymerase in colorectal tumours.

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“…These observations imply that also other unidentified positive/negative factors are effective in the proximal promoter of the CD97 gene (Shin et al, 2005). The construct -218/+45 carrying one GC-site showed the highest promoter activity whereas activity is almost abolished in the -111/+45 construct lacking GC-sequences.…”

Section: Discussionmentioning

confidence: 76%

“…We showed that Sp3 acts as transcriptional activator, like Sp1, in the proximal region of the CD97 promoter. This suggests that Sp1 and Sp3 cross-regulate the expression of each other which could be explained by the fact that the Sp3 protein is able to bind within the Sp1 promoter (Shin et al, 2005). Although Sp1 and Sp3 can bind to the same GC-rich box, Sp3 was originally found to suppress Sp1-mediated activation by binding to the this sequence, thereby preventing Sp1-binding and activation.…”

Section: Discussionmentioning

confidence: 99%

“…Several Sp proteins (Sp1-Sp8) have been identified (Bouwman and Philipsen, 2002;Suske et al, 2005). Whereas most Sp proteins show tissue-restricted expression patterns, Sp1 and Sp3 are ubiquitously expressed and compete for common target sequences (Shin et al, 2005). Sp1 is well known as a transcriptional activator, whereas Sp3 can be either a transcriptional activator or repressor of Sp1-mediated transcription, depending on the promoter context and cell type (Majello et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Transcriptional regulation of the human CD97 promoter by Sp1/Sp3 in smooth muscle cells

Wobus

Wandel

Prohaska

et al. 2008

Gene

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The EGF-TM7 receptor CD97 shows different features of expression and function in muscle cells compared to hematopoetic and tumor cells. Since the molecular function and regulation of CD97 is poorly understood, this study aimed at defining its basal transcriptional regulation in smooth muscle cells (SMCs).The computational analysis of the CD97 5'-flanking region revealed that the TATA boxlacking promoter possesses several GC-rich regions as putative Sp1/Sp3 binding sites.Transfection studies with serially deleted promoter constructs demonstrated that the minimal promoter fragment resided in the -218/+45 region containing one out of five identified GCboxes in the leiomyosarcoma cell line SK-LMS-1 and human bronchial smooth muscle cells (HbSMCs). Mutation of the most proximal GC-site in CD97 reporter gene constructs caused a significant decrease in promoter activity. Gel shift assays and chromatin immunoprecipitation revealed that Sp1 and Sp3 bound specifically to the most proximal GC-site. Furthermore, we showed that Sp1 and Sp3 over-expression activates CD97 promoter activity in HEK 293 cells.Our data characterize for the first time the activity of the human CD97 promoter which is controlled by Sp1/Sp3 transcription factors in SMCs.2

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Sp1 and Sp3 transcription factors upregulate the proximal promoter of the human prostate-specific antigen gene in prostate cancer cells

Cited by 21 publications

References 46 publications

Regulation of Histone Deacetylase 4 Expression by the SP Family of Transcription Factors

Regulation of Histone Deacetylase 4 Expression by the SP Family of Transcription Factors

Characterization of promoter regulatory elements involved in downexpression of the DNA polymerase κ in colorectal cancer

Transcriptional regulation of the human CD97 promoter by Sp1/Sp3 in smooth muscle cells

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