Evidence map›Paper›PMID 26857455›Full record

ArticleScientific reports2016

Small-molecule inhibition of PTPRZ reduces tumor growth in a rat model of glioblastoma.

Akihiro Fujikawa, Asako Nagahira, Hajime Sugawara, Kentaro Ishii, Seiichi Imajo, Masahito Matsumoto, Kazuya Kuboyama, Ryoko Suzuki, Naomi Tanga, Masanori Noda and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.7field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 57 citations in OpenAlex.

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  13. A novel PTPRZ1-ETV1 fusion in gliomas.Brain pathology (Zurich, Switzerland) · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 1 country.

Akihiro FujikawaDivision of Molecular Neurobiology, National Institute for Basic Biology (NIBB), 5-1 Higashiyama, Myodaiji-cho, Okazaki, Aichi, 444-8787, Japan.
Asako NagahiraAsubio Pharma Co., Ltd., 6-4-3 Minatojima-Minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
Hajime SugawaraAsubio Pharma Co., Ltd., 6-4-3 Minatojima-Minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
Kentaro IshiiDepartment of Bioorganization Research, Okazaki Institute for Integrative Bioscience, 5-1 Higashiyama, Myodaiji-cho, Okazaki, Aichi, 444-8787, Japan.
Seiichi ImajoAsubio Pharma Co., Ltd., 6-4-3 Minatojima-Minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
Masahito MatsumotoDivision of Molecular Neurobiology, National Institute for Basic Biology (NIBB), 5-1 Higashiyama, Myodaiji-cho, Okazaki, Aichi, 444-8787, Japan.
Kazuya KuboyamaDivision of Molecular Neurobiology, National Institute for Basic Biology (NIBB), 5-1 Higashiyama, Myodaiji-cho, Okazaki, Aichi, 444-8787, Japan.
Ryoko SuzukiDivision of Molecular Neurobiology, National Institute for Basic Biology (NIBB), 5-1 Higashiyama, Myodaiji-cho, Okazaki, Aichi, 444-8787, Japan.
Naomi TangaDivision of Molecular Neurobiology, National Institute for Basic Biology (NIBB), 5-1 Higashiyama, Myodaiji-cho, Okazaki, Aichi, 444-8787, Japan.
Masanori NodaDepartment of Biotechnology, Graduate School of Engineering, Osaka University, 2-1 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Susumu UchiyamaDepartment of Bioorganization Research, Okazaki Institute for Integrative Bioscience, 5-1 Higashiyama, Myodaiji-cho, Okazaki, Aichi, 444-8787, Japan.
Toshiyuki TomooAsubio Pharma Co., Ltd., 6-4-3 Minatojima-Minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
Atsuto OgataAsubio Pharma Co., Ltd., 6-4-3 Minatojima-Minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
Makoto MasumuraAsubio Pharma Co., Ltd., 6-4-3 Minatojima-Minamimachi, Chuo-ku, Kobe, Hyogo, 650-0047, Japan.
Masaharu NodaDivision of Molecular Neurobiology, National Institute for Basic Biology (NIBB), 5-1 Higashiyama, Myodaiji-cho, Okazaki, Aichi, 444-8787, Japan.
Kobe Asahi Hospital · JPNational Institute for Basic Biology · JPOsaka University · JPOkazaki Institute for Integrative Bioscience · JPThe Graduate University for Advanced Studies, SOKENDAI · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein tyrosine phosphatase receptor-type Z (PTPRZ) is aberrantly over-expressed in glioblastoma and a causative factor for its malignancy. However, small molecules that selectively inhibit the catalytic activity of PTPRZ have not been discovered. We herein performed an in vitro screening of a chemical library, and identified SCB4380 as the first potent inhibitor for PTPRZ. The stoichiometric binding of SCB4380 to the catalytic pocket was demonstrated by biochemical and mass spectrometric analyses. We determined the crystal structure of the catalytic domain of PTPRZ, and the structural basis of the binding of SCB4380 elucidated by a molecular docking method was validated by site-directed mutagenesis studies. The intracellular delivery of SCB4380 by liposome carriers inhibited PTPRZ activity in C6 glioblastoma cells, and thereby suppressed their migration and proliferation in vitro and tumor growth in a rat allograft model. Therefore, selective inhibition of PTPRZ represents a promising approach for glioma therapy.

Indexed as

Enzyme InhibitorsGlioblastomaMolecular Docking SimulationNeoplasm ProteinsNeoplasms, ExperimentalReceptor-Like Protein Tyrosine Phosphatases, Class 5AnimalsCell Line, TumorCrystallography, X-RayMaleMutagenesis, Site-DirectedRatsRats, WistarEnzyme InhibitorsNeoplasm ProteinsPtprz1 protein, ratReceptor-Like Protein Tyrosine Phosphatases, Class 5

Identifiers

PMID26857455
PMCPMC4746629
OpenAlexW2410036060

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Registered trials

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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.