ArticleOncogene2010
PBK/TOPK interacts with the DBD domain of tumor suppressor p53 and modulates expression of transcriptional targets including p21.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 116 citations in OpenAlex.
- Evidence for PDZ-Binding Kinase in Lung Disease With an Emphasis on PAH.Pulmonary circulation · 2026Review
- Advances in T-Lymphokine-activated Killer Cell-originated Protein Kinase Research in Cancer Over the Past Thirty Years.Journal of cancer prevention · 2026Review
- TOPK Suppresses the CD8Cancer communications (London, England) · 2026Article
- The Roles of TOPK in Tumorigenesis and Development: Structure, Mechanisms, Pathways, and Therapeutic Implications.International journal of biological sciences · 2026Review
- RBM15 aggravates endometrial cancer progression by inducing PBK m6A modification to inhibit the p53 pathway.Cytotechnology · 2025Article
- The oncogenic kinase TOPK upregulates in psoriatic keratinocytes and contributes to psoriasis progression by regulating neutrophils infiltration.Cell communication and signaling : CCS · 2024Article
- PDZ-Binding Kinase, a Novel Regulator of Vascular Remodeling in Pulmonary Arterial Hypertension.Circulation · 2024Article
- Transcriptomic Analysis of Pubertal and Adult Virgin Mouse Mammary Epithelial and Stromal Cell Populations.Journal of mammary gland biology and neoplasia · 2024Article
- The role and mechanism of PDZ binding kinase in hypobaric and hypoxic acute lung injury.Journal of thoracic disease · 2024Article
- Cancer testis antigens: Emerging therapeutic targets leveraging genomic instability in cancer.Molecular therapy. Oncology · 2024Review
- KRASJournal of cellular and molecular medicine · 2023Article
- A Review of the Regulatory Mechanisms of N-Myc on Cell Cycle.Molecules (Basel, Switzerland) · 2023Review
- Identification of potential biomarkers in cancer testis antigens for glioblastoma.American journal of translational research · 2023Article
- The design of TOPK inhibitors using structure-based pharmacophore modeling and molecular docking based on an MD-refined homology model.Molecular diversity · 2022Article
- Colorectal cancer concurrent gene signature based on coherent patterns between genomic and transcriptional alterations.BMC cancer · 2022Article
- The role of T-LAK cell-originated protein kinase in targeted cancer therapy.Molecular and cellular biochemistry · 2022Review
- Acetylshikonin suppresses diffuse large B-Cell Lymphoma cell growth by targeting the T-lymphokine-activated killer cell-originated protein kinase signalling pathway.Bioengineered · 2022Article
- High expression of PDZ-binding kinase is correlated with poor prognosis and immune infiltrates in hepatocellular carcinoma.World journal of surgical oncology · 2022Article
- Comprehensive analysis of differentially expressed genes reveals the promotive effects of UBE2T on colorectal cancer cell proliferation.Oncology letters · 2021Article
- Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PBK/TOPK (PDZ-binding kinase, T-LAK-cell-originated protein kinase) is a serine-threonine kinase that is overexpressed in a variety of tumor cells but its role in oncogenesis remains unclear. Here we show, by co-immunoprecipitation experiments and yeast two-hybrid analysis, that PBK/TOPK physically interacts with the tumor suppressor p53 through its DNA-binding (DBD) domain in HCT116 colorectal carcinoma cells that express wild-type p53. PBK also binds to p53 mutants carrying five common point mutations in the DBD domain. The PBK-p53 interaction appears to downmodulate p53 transactivation function as indicated by PBK/TOPK knockdown experiments, which show upregulated expression of the key p53 target gene and cyclin-dependent kinase inhibitor p21 in HCT116 cells, particularly after genotoxic damage from doxorubicin. Furthermore, stable PBK/TOPK knockdown cell lines (derived from HCT116 and MCF-7 cells) showed increased apoptosis, G(2)/M arrest and slower growth as compared to stable empty vector-transfected control cell lines. Gene microarray studies identified additional p53 target genes involved in apoptosis or cell cycling, which were differentially regulated by PBK knockdown. Together, these data suggest that increased levels of PBK/TOPK may contribute to tumor cell development and progression through suppression of p53 function and consequent reductions in the cell-cycle regulatory proteins such as p21. PBK/TOPK may therefore be a valid target for antineoplastic kinase inhibitors to sensitize tumor cells to chemotherapy-induced apoptosis and growth suppression.
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