ArticleMolecular cancer2015
Targeting PBK/TOPK decreases growth and survival of glioma initiating cells in vitro and attenuates tumor growth in vivo.
Article in Molecular cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
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Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Systematic Review of Molecular Targeted Therapies for Adult-Type Diffuse Glioma: An Analysis of Clinical and Laboratory Studies.International journal of molecular sciences · 2023Pooled it
- PDZ-binding kinase promotes ovarian cancer cell proliferation and invasion viaTranslational cancer research · 2026Article
- Elevated Plasma T-LAK cell-originated protein kinase Owned the Potential for Predicting Favorable Outcomes in Acute Ischemic Stroke Patients.Cellular and molecular neurobiology · 2026Article
- The Roles of TOPK in Tumorigenesis and Development: Structure, Mechanisms, Pathways, and Therapeutic Implications.International journal of biological sciences · 2026Review
- Targeting PBK with small-molecule 1-Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Machine learning approach identifies inflammatory gene signature for predicting survival outcomes in hepatocellular carcinoma.Scientific reports · 2024Article
- Unraveling the role of PBK in glioblastoma: from molecular mechanisms to therapeutic targets.Annals of medicine and surgery (2012) · 2024Article
- Unveiling the significance of cancer-testis antigens and their implications for immunotherapy in glioma.Discover oncology · 2024Review
- Decoding the immune microenvironment: unveiling CD8 + T cell-related biomarkers and developing a prognostic signature for personalized glioma treatment.Cancer cell international · 2024Article
- The oncogenic kinase TOPK upregulates in psoriatic keratinocytes and contributes to psoriasis progression by regulating neutrophils infiltration.Cell communication and signaling : CCS · 2024Article
- The role and mechanism of PDZ binding kinase in hypobaric and hypoxic acute lung injury.Journal of thoracic disease · 2024Article
- Comprehensive Analysis of the Mechanism of Anoikis in Hepatocellular Carcinoma.Genetics research · 2024Article
- Molecular Targeted Therapies in Glioblastoma Multiforme: A Systematic Overview of Global Trends and Findings.Brain sciences · 2023Review
- Identification of CDK1, PBK, and CHEK1 as an Oncogenic Signature in Glioblastoma: A Bioinformatics Approach to Repurpose Dapagliflozin as a Therapeutic Agent.International journal of molecular sciences · 2023Article
- The LIN28B-let-7-PBK pathway is essential for group 3 medulloblastoma tumor growth and survival.Molecular oncology · 2023Article
- Specific Regulation of mGenomics, proteomics & bioinformatics · 2023Article
- TOPK promotes the growth of esophageal cancer in vitro and in vivo by enhancing YB1/eEF1A1 signal pathway.Cell death & disease · 2023Article
- The peritumoral brain zone in glioblastoma: where we are and where we are going.Journal of neuroscience research · 2023Review
- Identification of potential biomarkers in cancer testis antigens for glioblastoma.American journal of translational research · 2023Article
- Identification of a Fibroblast-Related Prognostic Model in Glioma Based on Bioinformatics Methods.Biomolecules · 2022Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastomas are invasive therapy resistant brain tumors with extremely poor prognosis. The Glioma initiating cell (GIC) population contributes to therapeutic resistance and tumor recurrence. Targeting GIC-associated gene candidates could significantly impact GBM tumorigenicity. Here, we investigate a protein kinase, PBK/TOPK as a candidate for regulating growth, survival and in vivo tumorigenicity of GICs.
methodsPBK is highly upregulated in GICs and GBM tissues as shown by RNA and protein analyses. We knocked down PBK using shRNA vectors and inhibited the function of PBK protein with a pharmacological PBK inhibitor, HITOPK-032. We assessed viability, tumorsphere formation and apoptosis in three patient derived GIC cultures.
resultsGene knockdown of PBK led to decreased viability and sphere formation and in one culture an increase in apoptosis. Treatment of cells with inhibitor HITOPK-032 (5 μM and 10 μM) almost completely abolished growth and elicited a large increase in apoptosis in all three cultures. HI-TOPK-032 treatment (5 mg/kg and 10 mg/kg bodyweight) in vivo resulted in diminished growth of experimentally induced subcutaneous GBM tumors in mice. We also carried out multi-culture assays of cell survival to investigate the relative effects on GICs compared with the normal neural stem cells (NSCs) and their differentiated counterparts. Normal NSCs seemed to withstand treatment slightly better than the GICs.
conclusionOur study of identification and functional validation of PBK suggests that this candidate can be a promising molecular target for GBM treatment.
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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.