ArticleScientific reports2017
Targeting PTPRZ inhibits stem cell-like properties and tumorigenicity in glioblastoma cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 79 citations in OpenAlex.
- The role of classical protein tyrosine phosphatases in diabetic kidney disease and therapeutic implications.Journal of biomedical science · 2026Review
- Development and Characterization of a Patient-DerivedJTO clinical and research reports · 2026Article
- Patient-derived organoids predict personalized drug response and reveal alternative therapeutic options in glioblastoma.Cell reports. Medicine · 2026Article
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- Dysregulation of post-translational modifications in glioma: advances in pathological mechanisms and clinical targeting strategies.Journal of translational medicine · 2026Review
- Human organoid tumor transplantation identifies functional glioblastoma-microenvironment communication mediated by PTPRZ1.Cell reports · 2026Article
- Defining the extracellular matrix for targeted immunotherapy in adult and pediatric brain cancer.NPJ precision oncology · 2025Article
- KAT5 regulates neurodevelopmental states associated with G0-like populations in glioblastoma.Nature communications · 2025Article
- Vaccine-induced T cell receptor T cell therapy targeting a glioblastoma stemness antigen.Nature communications · 2025Article
- Mechanisms of GPM6A in Malignant Tumors.Cancer reports (Hoboken, N.J.) · 2025Review
- Single-cell profiling uncovers PTPRG-driven stemness in malignant plasma cells and signatures of treatment failure in multiple myeloma.Frontiers in immunology · 2025Article
- Article
- HSV1 microRNAs in glioblastoma development: an in silico study.Scientific reports · 2024Article
- Sequence - dynamics - function relationships in protein tyrosine phosphatases.QRB discovery · 2024Article
- Inhibition of exosome biogenesis affects cell motility in heterogeneous sub-populations of paediatric-type diffuse high-grade gliomas.Cell & bioscience · 2023Article
- Genetic deletion or tyrosine phosphatase inhibition of PTPRZ1 activates c-Met to up-regulate angiogenesis and lung adenocarcinoma growth.International journal of cancer · 2023Article
- Distinct Lineage of Slow-Cycling Cells Amidst the Prevailing Heterogeneity in Glioblastoma.Cancers · 2023Article
- Partial male-to-female reprogramming of mouse fetal testis by Sertoli cell ablation.Development (Cambridge, England) · 2023Article
- Protein Tyrosine Phosphatase Receptor Zeta 1 as a Potential Target in Cancer Therapy and Diagnosis.International journal of molecular sciences · 2023Review
- Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The R5 subfamily of receptor-type protein tyrosine phosphatases (RPTPs) comprises PTPRZ and PTPRG. A recent study on primary human glioblastomas suggested a close association between PTPRZ1 (human PTPRZ) expression and cancer stemness. However, the functional roles of PTPRZ activity in glioma stem cells have remained unclear. In the present study, we found that sphere-forming cells from the rat C6 and human U251 glioblastoma cell lines showed high expression levels of PTPRZ-B, the short receptor isoform of PTPRZ. Stable PTPRZ knockdown altered the expression levels of stem cell transcription factors such as SOX2, OLIG2, and POU3F2 and decreased the sphere-forming abilities of these cells. Suppressive effects on the cancer stem-like properties of the cells were also observed following the knockdown of PTPRG. Here, we identified NAZ2329, a cell-permeable small molecule that allosterically inhibits both PTPRZ and PTPRG. NAZ2329 reduced the expression of SOX2 in C6 and U251 cells and abrogated the sphere-forming abilities of these cells. Tumor growth in the C6 xenograft mouse model was significantly slower with the co-treatment of NAZ2329 with temozolomide, an alkylating agent, than with the individual treatments. These results indicate that pharmacological inhibition of R5 RPTPs is a promising strategy for the treatment of malignant gliomas.
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