Identification of PTPRZ as a drug target for cancer stem cells in glioblastoma
- Date:
- July 18, 2017
- Source:
- National Institutes of Natural Sciences
- Summary:
- Scientists have shown that the enzymatic activity of PTPRZ is requisite for the maintenance of stem cell properties and tumorigenicity in glioblastoma cells.
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Glioblastoma is the most malignant brain tumor with high mortality. Cancer stem cells are thought to be crucial for tumor initiation and its recurrence after standard therapy with radiation and temozolomide (TMZ) chemotherapy. Protein tyrosine phosphatase receptor type Z (PTPRZ) is an enzyme that is highly expressed in glioblastoma, especially in cancer stem cells.
The research group of Professor Masaharu Noda and Researcher Akihiro Fujikawa of the National Institute for Basic Biology (NIBB) showed that the enzymatic activity of PTPRZ is requisite for the maintenance of stem cell properties and tumorigenicity in glioblastoma cells. PTPRZ knockdown strongly inhibited tumor growth of C6 glioblastoma cells in a mouse xenograft model.
In addition, the research team discovered NAZ2329, an allosteric inhibitor of PTPRZ, in collaboration with ASUBIO Pharma Co. Ltd.. NAZ2329 efficiently suppressed stem cell-like properties of glioblastoma cells in culture, and tumor growth in C6 glioblastoma xenografts. These results indicate that pharmacological inhibition of PTPRZ is a promising strategy for the treatment of malignant gliomas.
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Materials provided by National Institutes of Natural Sciences. Note: Content may be edited for style and length.
Journal Reference:
- Akihiro Fujikawa, Hajime Sugawara, Taisaku Tanaka, Masahito Matsumoto, Kazuya Kuboyama, Ryoko Suzuki, Naomi Tanga, Atsuto Ogata, Makoto Masumura, Masaharu Noda. Targeting PTPRZ inhibits stem cell-like properties and tumorigenicity in glioblastoma cells. Scientific Reports, 2017; 7 (1) DOI: 10.1038/s41598-017-05931-8
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