Evidence map›Paper›PMID 33409495›Full record

ArticleNeuro-oncology advances

Rab27b contributes to radioresistance and exerts a paracrine effect via epiregulin in glioblastoma.

Soichiro Nishioka, Ping-Hsiu Wu, Toshiaki Yakabe, Amato J Giaccia, Quynh-Thu Le, Hidefumi Aoyama, Shinichi Shimizu, Hiroki Shirato, Yasuhito Onodera, Jin-Min Nam

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In one paragraph

Article in Neuro-oncology advances. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
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  7. The Role of EREG/EGFR Pathway in Tumor Progression.International journal of molecular sciences · 2021
    Review
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

10 authors at 3 institutions in 2 countries.

Soichiro NishiokaMolecular and Cellular Dynamics Research, Graduate School of Biomedical Science and Engineering, Hokkaido University, Sapporo, Japan.
Ping-Hsiu WuGlobal Center for Biomedical Science and Engineering, Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Toshiaki YakabeSchool of Medicine, Hokkaido University, Sapporo, Japan.
Amato J GiacciaDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, California, USA.
Quynh-Thu LeDepartment of Radiation Oncology, Stanford University School of Medicine, Stanford, California, USA.
Hidefumi AoyamaDepartment of Radiation Oncology, Faculty of Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0002-8437-7491
Shinichi ShimizuGlobal Center for Biomedical Science and Engineering, Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Hiroki ShiratoGlobal Center for Biomedical Science and Engineering, Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Yasuhito OnoderaGlobal Center for Biomedical Science and Engineering, Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Jin-Min NamGlobal Center for Biomedical Science and Engineering, Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Hokkaido University · JPStanford University · USSapporo Medical University · JP

Funding

Cancer Research UK 28736
6 · The paper itself

Abstract

backgroundRadiotherapy is the standard treatment for glioblastoma (GBM). However, radioresistance of GBM cells leads to recurrence and poor patient prognosis. Recent studies suggest that secretion factors have important roles in radioresistance of tumor cells. This study aims to determine whether Rab27b, a small GTPase involved in secretory vesicle trafficking, plays a role in radioresistance of GBM.

methodsMicroarray analysis, cell viability analysis, apoptosis assay, immunostaining, and in vivo experiments were performed to assess the effect of Rab27b on radioresistance of GBM. We further investigated paracrine effects mediated by Rab27b after X-ray irradiation using coculture systems of glioma cell lines.

resultsRab27b was specifically upregulated in irradiated U87MG cells. Furthermore, Rab27b knockdown decreased the proliferation of GBM cells after irradiation. Knockdown of Rab27b in U87MG cells combined with radiation treatment suppressed orthotopic tumor growth in the mouse brain and prolonged the survival of recipient mice. Interestingly, the co-upregulation of Rab27b and epiregulin (EREG), a member of the epidermal growth factor (EGF) family, correlated with radioresistance in glioma cell lines. Additionally, EREG, which was secreted from U87MG cells via Rab27b-mediated mechanism, activated EGF receptor and contributed to H4 cell proliferation in a paracrine manner.

conclusionsOur results show that Rab27b mediates the radioresistance of highly malignant GBM cells. Rab27b promotes the proliferation of adjacent cells through EREG-mediated paracrine signaling after irradiation. Thus, the Rab27b-EREG pathway is a novel potential target to improve the efficacy of radiotherapy in GBM.

Indexed as

epiregulinglioblastomaparacrineRab27bradioresistance

Identifiers

PMID33409495
PMCPMC7770522
OpenAlexW3047925725

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.