ArticleOncotarget2015
PBK/TOPK enhances aggressive phenotype in prostate cancer via β-catenin-TCF/LEF-mediated matrix metalloproteinases production and invasion.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
40 citing papers in PubMed, 62 citations in OpenAlex.
- Molecular regulation of estrogen receptors and recent advances on ERα36 splice variant in prostate cancer.Journal of the Endocrine Society · 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
- Article
- The Roles of TOPK in Tumorigenesis and Development: Structure, Mechanisms, Pathways, and Therapeutic Implications.International journal of biological sciences · 2026Review
- Construction and validation of a lysine beta hydroxybutyrylation related molecular model for predicting biochemical recurrence of prostate cancer.Scientific reports · 2025Article
- Mitochondrial unfolded protein response-dependent β-catenin signaling promotes neuroendocrine prostate cancer.Oncogene · 2025Article
- TOPK Inhibition Enhances the Sensitivity of Colorectal Cancer Cells to Radiotherapy by Reducing the DNA Damage Response.Current medical science · 2024Article
- Transcriptome Analysis of Beta-Catenin-Related Genes in CD34+ Haematopoietic Stem and Progenitor Cells from Patients with AML.Mediterranean journal of hematology and infectious diseases · 2024Article
- The peritumoral brain zone in glioblastoma: where we are and where we are going.Journal of neuroscience research · 2023Review
- The role of the SGK3/TOPK signaling pathway in the transition from acute kidney injury to chronic kidney disease.Frontiers in pharmacology · 2023Article
- An in-silico approach leads to explore six genes as a molecular signatures of lung adenocarcinoma.American journal of cancer research · 2023Article
- Novel Paired Normal Prostate and Prostate Cancer Model Cell Systems Derived from African American Patients.Cancer research communications · 2022Article
- The role of T-LAK cell-originated protein kinase in targeted cancer therapy.Molecular and cellular biochemistry · 2022Review
- T-LAK cell-originated protein kinase (TOPK): an emerging prognostic biomarker and therapeutic target in osteosarcoma.Molecular oncology · 2021Article
- PBK expression predicts favorable survival in colorectal cancer patients.Virchows Archiv : an international journal of pathology · 2021Article
- Targeting Feedforward Loops Formed by Nuclear Receptor RORγ and Kinase PBK in mCRPC with Hyperactive AR Signaling.Cancers · 2021Article
- Review
- PBK Enhances Cellular Proliferation With Histone H3 Phosphorylation and Suppresses Migration and Invasion With CDH1 Stabilization in Colorectal Cancer.Frontiers in pharmacology · 2021Article
- T-LAK cell-originated protein kinase (TOPK) is a Novel Prognostic and Therapeutic Target in Chordoma.Cell proliferation · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
A current challenge in prostate cancer treatment is how to differentiate aggressive disease from indolent prostate cancer. There is an urgent need to identify markers that would accurately distinguish indolent prostate cancer from aggressive disease. The aim of this study was to evaluate the role of PDZ Domain-binding kinase (PBK) in prostate cancer and to determine if PBK expression enhances aggressiveness in prostate cancer. Using archival tissue samples, gain-of-function and loss-of-function studies, we show that PBK expression is up-regulated in prostate cancer, and its expression level is commensurate with invasiveness. Modulation of PBK expression and function causally regulates the invasive ability of prostate cancer cells. Production of matrix metalloproteinases-2 and -9, which are key players in metastatic invasion, is up-regulated, and the promoters of these genes are transcriptionally activated by PBK via increased β-catenin-TCF/LEF signaling. Prostate cancer tissue specimens show that PBK's expression correlates with aggressive disease and distant metastasis in bone, lymph node and abdomen. Our in vitro and in situ data are in agreement that PBK could be a prognostic biomarker for prostate cancer that would discriminate aggressive prostate cancer from indolent disease, and is a potential target for the therapeutic intervention of aggressive prostate cancer in men.
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Registered trials
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.