ArticleOncogene2007
PBK/TOPK promotes tumour cell proliferation through p38 MAPK activity and regulation of the DNA damage response.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 143 citations in OpenAlex.
- PDZ-binding kinase promotes ovarian cancer cell proliferation and invasion viaTranslational cancer research · 2026Article
- 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
- The Roles of TOPK in Tumorigenesis and Development: Structure, Mechanisms, Pathways, and Therapeutic Implications.International journal of biological sciences · 2026Review
- Pbk positively regulates myoblast differentiation and muscle regeneration via enhancing AMPK/ULK1 mediated myogenic autophagy.Journal of translational medicine · 2025Article
- Integrated Multi-Omics Profiling Identifies PDZ-Binding Kinase (PBK) as a Novel Prognostic Biomarker in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2025Article
- Unraveling the role of PBK in glioblastoma: from molecular mechanisms to therapeutic targets.Annals of medicine and surgery (2012) · 2024Article
- PDZ-Binding Kinase, a Novel Regulator of Vascular Remodeling in Pulmonary Arterial Hypertension.Circulation · 2024Article
- Machine-learning-based classification of diffuse large B-cell lymphoma patients by a 7-mRNA signature enriched with immune infiltration and cell cycle.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Article
- The role and mechanism of PDZ binding kinase in hypobaric and hypoxic acute lung injury.Journal of thoracic disease · 2024Article
- Article
- Specific Regulation of mGenomics, proteomics & bioinformatics · 2023Article
- An in-silico approach leads to explore six genes as a molecular signatures of lung adenocarcinoma.American journal of cancer research · 2023Article
- Overexpression of PBK/TOPK relates to poor prognosis of patients with breast cancer: a retrospective analysis.World journal of surgical oncology · 2022Article
- Identification of PBK as a hub gene and potential therapeutic target for medulloblastoma.Oncology reports · 2022Article
- The role of T-LAK cell-originated protein kinase in targeted cancer therapy.Molecular and cellular biochemistry · 2022Review
- PBK/TOPK Is a Favorable Prognostic Biomarker Correlated with Antitumor Immunity in Colon Cancers.Biomedicines · 2022Article
- T-LAK cell-originated protein kinase (TOPK): an emerging prognostic biomarker and therapeutic target in osteosarcoma.Molecular oncology · 2021Article
- Menin-regulated Pbk controls high fat diet-induced compensatory beta cell proliferation.EMBO molecular medicine · 2021Article
- Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The contribution of the insulin-like growth-factor-I receptor (IGF-IR) to tumour progression is well documented. To identify new mediators of IGF-IR function in cancer, we recently isolated genes differentially expressed in cells overexpressing the IGF-IR. Among these was the serine/threonine kinase PBK/TOPK (PDZ-binding kinase/T-LAK cell-originated protein kinase), previously associated with highly proliferative cells and tissues. Here, we show that PBK is expressed at high levels in tumour cell lines compared with non-transformed cells. IGF-I could induce PBK expression only in transformed cells, whereas epidermal growth factor could induce PBK in non-transformed MCF-10A breast epithelial cells. Suppression of PBK expression using small interfering RNA did not prevent progression through the cell cycle, but caused decreased proliferation over time in culture, and reduced clonogenic growth in soft agarose. PBK knockdown impaired p38 activation after long-term stimulation with different growth factors and reduced DU145 cells motility. Suppressed PBK expression also resulted in an impaired response to DNA damage that was evident by the decreased generation of gamma-H2AX, increased DNA damage and decreased cell survival. Taken together, the data indicate that PBK is necessary for appropriate activation and function of the p38 pathway by growth factors. Thus, enhanced expression of PBK may facilitate tumour growth by mediating p38 activation and by helping cells to overcome DNA damage.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.