Evidence map›Paper›PMID 42534262›Full record

ArticleMolecular and clinical oncology2026

Differentiation therapy targeting indoleamine 2,3-dioxygenase 1 in glioblastoma cells

Kaoru Nishide, Shun Yamamuro, Yumi Aida, Yoshinari Ozawa, Emiko Sano, Atsuo Yoshino

Abstract read
In one paragraph

Article in Molecular and clinical oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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.

2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Kaoru NishideDepartment of Neurological Surgery, Nihon University School of Medicine, Tokyo 173-8610, Japan.
Shun YamamuroDepartment of Neurological Surgery, Nihon University School of Medicine, Tokyo 173-8610, Japan.
Yumi AidaDepartment of Neurological Surgery, Nihon University School of Medicine, Tokyo 173-8610, Japan.
Yoshinari OzawaDepartment of Neurological Surgery, Nihon University School of Medicine, Tokyo 173-8610, Japan.
Emiko SanoDepartment of Neurological Surgery, Nihon University School of Medicine, Tokyo 173-8610, Japan.
Atsuo YoshinoDepartment of Neurological Surgery, Nihon University School of Medicine, Tokyo 173-8610, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma cells strongly express the tryptophan-metabolizing enzyme indoleamine 2,3-dioxygenase 1 (IDO1), which is important in enabling immune evasion. Notably, glioma stem-like cells (GSCs) express higher levels of IDO1 than differentiated glioblastoma cells (DGCs); therefore, it was hypothesized that IDO1 inhibition in GSCs may induce differentiation. The present study used the glioblastoma cell line U-87MG, and newly established GSC lines 0125-GSC and 0222-GSC. A model GSC line, Rev-U-87MG, was created by culturing U-87MG in serum-free medium. Rev-U-87MG-IDO(-) was generated by continuous treatment with an IDO1 inhibitor. The DGC lines 0125-DGC and 0222-DGC were derived by culturing 0125-GSC and 0222-GSC in serum-containing medium. IDO1-inhibited GSC lines 0125-GSC-IDO(-) and 0222-GSC-IDO(-) were generated by continuous IDO1 inhibitor exposure. The expression levels of IDO1 and stem cell markers (Nestin, Nanog and Sox2) were measured by western blotting, and temozolomide sensitivity was evaluated by cell counting. Notably, U-87MG, 0125-DGC and 0222-DGC adhered without sphere formation. By contrast, Rev-U-87MG, 0125-GSC and 0222-GSC formed spheres, whereas IDO1-inhibited cells showed partial adhesion with reduced sphere formation. IDO1 and stem cell marker expression were reduced in all IDO1-inhibited cell lines. Rev-U-87MG exhibited decreased temozolomide sensitivity compared with U-87MG, whereas Rev-U-87MG-IDO(-) showed increased sensitivity. Similarly, 0125-DGC and 0222-DGC were more sensitive than their parent GSC lines, and 0125-GSC-IDO(-) and 0222-GSC-IDO(-) also exhibited enhanced drug sensitivity compared with their parent GSC lines at multiple concentrations. These findings suggest that IDO1 inhibition may induce the differentiation of GSCs and reduce their resistance to temozolomide.

Indexed as

3-dioxygenase 1differentiation therapyglioblastomaglioma stem-like cellsindoleamine 2in vitro

Identifiers

PMID42534262
PMCPMC13419861

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