Evidence map›Paper›PMID 41378763›Full record

ArticleAutophagy2026

NK cell-derived GZMB (granzyme B) suppresses glioblastoma radioresistance by blocking SDC1-mediated autophagosome maturation.

Jingze Yan, Ruishen Feng, Qin Qin, Gefenqiang Shen, Meng Tian, Sunkai Ling, Shu Zhou, Fei Li, Xiaojie Xia, Yuandong Cao and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Autophagy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

14 authors.

Jingze YanDepartment of Radiation Oncology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Ruishen FengDepartment of Radiation Oncology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Qin QinDepartment of Radiation Oncology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Gefenqiang ShenDepartment of Radiation Oncology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Meng TianDepartment of Radiation Oncology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Sunkai LingDepartment of Radiation Oncology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Shu ZhouDepartment of Radiation Oncology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Fei LiDepartment of Radiation Oncology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Xiaojie XiaDepartment of Radiation Oncology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Yuandong CaoDepartment of Radiation Oncology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Liang ZengInstitution of Radiation Medicine, Shanghai Medical College, Fudan University, Shanghai, China.
Chunlin ShaoInstitution of Radiation Medicine, Shanghai Medical College, Fudan University, Shanghai, China.
Xinchen SunDepartment of Radiation Oncology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Wang ZhengDepartment of Radiation Oncology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiotherapy is a fundamental step in the combined treatment of glioblastoma (GBM), while radioresistance of GBM causes limitation of therapeutic efficacy. Natural killer (NK) cells, a potential target of immunotherapy, have attracted considerable attention due to the robust cancer cell-targeted cytotoxicity in combined treatment with radiotherapy, suggesting NK cell regulation might be a radiosensitization strategy. Here we show that a cytotoxic subset of NK cells could be stimulated by ionizing radiation (IR) and accumulate in the GBM tumor microenvironment (TME). Co-culturing with NK cells significantly enhances the GBM cell response to IR, and pharmaceutically depleting NK cells in mice elevates IR-induced tumor growth delay. Specifically, GZMB should be the radiosensitization effector secreted by NK cells. Suppressing GZMB activity remarkably impairs NK-mediated GBM radiosensitization. Meanwhile, administrating exogenous GZMB improves irradiation dose-survival response in

Indexed as

AutophagosomesBrain NeoplasmsGlioblastomaGranzymesKiller Cells, NaturalRadiation ToleranceAnimalsAutophagyCell Line, TumorHumansLysosomesMiceTumor MicroenvironmentGranzymesAutophagosome maturationglioblastomagranzyme Bnatural killer cellradiosensitivitysyndecan 1

Identifiers

PMID41378763
PMCPMC12931911

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.