Promoter cloning and characterization of the human programmed cell death protein 4 (pdcd4) gene: evidence for ZBP-89 and Sp-binding motifs as essential Pdcd4 regulators
Abstract
Pdcd4 (programmed cell death protein 4) is an important novel tumour suppressor inhibiting transformation, translation, invasion and intravasation, and its expression is down-regulated in several cancers. However, little is known about the transcriptional regulation and the promoter of this important tumour suppressor. So far the following is the first comprehensive study to describe the regulation of Pdcd4 transcription by ZBP-89 (zinc-finger-binding protein 89), besides characterizing the gene promoter. We identified the transcriptional start sites of the human pdcd4 promoter, a functional CCAAT-box, and the basal promoter region. Within this basal region, computer-based analysis revealed several potential binding sites for ZBPs, especially for Sp (specificity protein) family members and ZBP-89. We identified four Sp1/Sp3/Sp4-binding elements to be indispensable for basal promoter activity. However, overexpression of Sp1 and Sp3 was not sufficient to enhance Pdcd4 protein expression. Analysis in different solid cancer cell lines showed a significant correlation between pdcd4 and zbp-89 mRNA amounts. In contrast with Sp transcription factors, overexpression of ZBP-89 led to an enhanced expression of Pdcd4 mRNA and protein. Additionally, specific knockdown of ZBP-89 resulted in a decreased pdcd4 gene expression. Reporter gene analysis showed a significant up-regulation of basal promoter activity by co-transfection with ZBP-89, which could be abolished by mithramycin treatment. Predicted binding of ZBP-89 to the basal promoter was confirmed by EMSA (electrophoretic mobility-shift assay) data and supershift analysis for ZBP-89. Taken together, data for the first time implicate ZBP-89 as a regulator of Pdcd4 by binding to the basal promoter either alone or by interacting with Sp family members.
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PDCD4 expression is controlled by zinc-finger protein transcription factors such as Sp and ZBP-89.
“The expression of PDCD4 was shown to be controlled by zinc-finger protein (ZBP) transcription factors such as specificity protein (Sp) and ZBP-89 [49].”
From Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions (2019) · cites this paper as [49]
Four Sp1/Sp3/Sp4-binding elements are indispensable for basal PDCD4 promoter activity, but overexpression of Sp1 and Sp3 is not sufficient to enhance PDCD4 expression; ZBP-89 is also needed.
“Leupold et al. [49] identified four Sp1/Sp3/Sp4-binding elements that are indispensable for basal promotor activity but the overexpression of Sp1 and Sp3 was not sufficient to enhance PDCD4 expression and ZBP-89 is also needed for PDCD4 expression.”
From Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions (2019) · cites this paper as [49]
ZBP-89 enhances PDCD4 expression by binding to the basal promoter region either alone or by interacting with Sp family members.
“ZBP-89 enhances PDCD4 expression by binding to the basal promotor region either alone or by interacting with Sp family members [49].”
From Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions (2019) · cites this paper as [49]
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Yao, X., Xu, K., Tao, N., Cheng, S., Chen, H., Zhang, D., Yang, M., Tan, M., Yu, H., Chen, P., et al. (2024) · Figshare · doi:10.6084/m9.figshare.25124091
Additional file 1 of ZNF148 inhibits HBV replication by downregulating RXRα transcription
Yao, X., Xu, K., Tao, N., Cheng, S., Chen, H., Zhang, D., Yang, M., Tan, M., Yu, H., Chen, P., et al. (2024) · Figshare · doi:10.6084/m9.figshare.25123983
Additional file 3 of ZNF148 inhibits HBV replication by downregulating RXRα transcription
Yao, X., Xu, K., Tao, N., Cheng, S., Chen, H., Zhang, D., Yang, M., Tan, M., Yu, H., Chen, P., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26675234
Programmed cell death protein 4 (PDCD4): a pleiotropic regulator in cardiovascular diseases
Zheng, M., & Jiang, X. (2026) · Journal of Physiology and Biochemistry · doi:10.1007/s13105-026-01237-4
- Authors
- Leupold, J. H., Asangani, I. A., Mudduluru, G., & Allgayer, H.
- Affiliations
- Department of Experimental Surgery, Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Germany
- University of Michigan (US)
- German Cancer Research Center (DE)
- Corresponding author
- Mudduluru, Giridhar
- Allgayer, Heike
- Venue
- Bioscience Reports
- Publisher
- Portland Press Ltd.
- Published
- 2012-01-30
- Volume
- 32
- Issue
- 3
- Pages
- 281-297
- ISSN
- 0144-8463 (ISSN-L)
- 1573-4935
- OpenAlex
- W2331935945
- Cited by
- 23
- References
- 76
- Citations by year
- 2026: 1 · 2024: 4 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 2 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 4 · 2013: 3
- FWCI
- 0.91
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Bioscience Reports (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Keywords
- PDCD4, ZBP-89, Sp transcription factors, Sp1, Sp3, Sp4, promoter regulation, transcriptional regulation, tumor suppressor, CCAAT box, transcription factor binding sites, mithramycin, gene knockdown, cancer cell lines
- MeSH terms
- Base Sequence, Binding Sites, DNA-Binding Proteins, Gene Expression Regulation, Humans, Plicamycin, Molecular Sequence Data, Promoter Regions, Genetic, Protein Binding, Protein Synthesis Inhibitors, Transcription Factors, Transcription, Genetic, RNA-Binding Proteins, Sequence Analysis, DNA, CCAAT-Binding Factor, Transcription Initiation Site, Cell Line, Tumor, Apoptosis Regulatory Proteins, Sp Transcription Factors
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