Evidence map›Paper›PMID 35778531›Full record

ArticleCell regeneration (London, England)2022

Interferon-beta inhibits human glioma stem cell growth by modulating immune response and cell cycle related signaling pathways.

Xin-Xin Han, Shengkai Jin, Li-Ming Yu, Min Wang, Xin-Yu Hu, Dai-Yu Hu, Jie Ren, Meng-Han Zhang, Wei Huang, Jia-Jia Deng and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Cell regeneration (London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
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  8. Review
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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

14 authors at 7 institutions in 1 country.

Xin-Xin Han *Shanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Shanghai Stomatological Hospital & School of Stomatology, Fudan University, Shanghai, China. xxhan@fudan.edu.cn.
Shengkai Jin *Institute of Photomedicine, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, China.
Li-Ming YuShanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Shanghai Stomatological Hospital & School of Stomatology, Fudan University, Shanghai, China.
Min WangSchool of Medicine, Jiaxing University, Jiaxing, China.
Xin-Yu HuTongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
Dai-Yu HuTongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
Jie RenTongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
Meng-Han ZhangShanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Shanghai Stomatological Hospital & School of Stomatology, Fudan University, Shanghai, China.
Wei HuangShanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Shanghai Stomatological Hospital & School of Stomatology, Fudan University, Shanghai, China.
Jia-Jia DengShanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Shanghai Stomatological Hospital & School of Stomatology, Fudan University, Shanghai, China.
Qing-Qing ChenShanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Shanghai Stomatological Hospital & School of Stomatology, Fudan University, Shanghai, China.
Zhengliang GaoTongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
Hua HeDepartment of Neurosurgery, Changzheng Hospital, Second Military Medical University, Shanghai, China. hehua1624@smmu.edu.cn.
Chunhui CaiTongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China. pattycaich@tongji.edu.cn.
Fudan University · CNShanghai Stomatological Hospital · CNShanghai Tenth People's Hospital · CNTongji University · CNJiaxing University · CNSecond Military Medical University · CNShanghai Skin Disease Hospital · CN

Funding

Key Technologies Research and Development Program 2019YFA0110300National Natural Science Foundation of China 31571058National Natural Science Foundation of China 31600819National Natural Science Foundation of China 32070862National Natural Science Foundation of China 81901031Natural Science Foundation of Shanghai 19ZR1445400Program for Professor of Special Appointment (Eastern Scholar) at Shanghai Institutions of Higher Learning 8101219003Shanghai Municipal Population and Family Planning Commission 20174Y0216
6 · The paper itself

Abstract

Malignant Glioma is characterized by strong self-renewal potential and immature differentiation potential. The main reason is that malignant glioma holds key cluster cells, glioma stem cells (GSCs). GSCs contribute to tumorigenesis, tumor progression, recurrence, and treatment resistance. Interferon-beta (IFN-β) is well known for its anti-proliferative efficacy in diverse cancers. IFN-β also displayed potent antitumor effects in malignant glioma. IFN-β affect both GSCs and Neural stem cells (NSCs) in the treatment of gliomas. However, the functional comparison, similar or different effects of IFN-β on GSCs and NSCs are rarely reported. Here, we studied the similarities and differences of the responses to IFN-β between human GSCs and normal NSCs. We found that IFN-β preferentially inhibited GSCs over NSCs. The cell body and nucleus size of GSCs increased after IFN-β treatment, and the genomic analysis revealed the enrichment of the upregulated immune response, cell adhesion genes and down regulated cell cycle, ribosome pathways. Several typical cyclin genes, including cyclin A2 (CCNA2), cyclin B1 (CCNB1), cyclin B2 (CCNB2), and cyclin D1 (CCND1), were significantly downregulated in GSCs after IFN-β stimulation. We also found that continuous IFN-β stimulation after passage further enhanced the inhibitory effect. Our study revealed how genetic diversity resulted in differential effects in response to IFN-β treatment. These results may contribute to improve the applications of IFN-β in anti-cancer immunotherapy. In addition, these results may also help to design more effective pharmacological strategies to target cancer stem cells while protecting normal neural stem cells.

Indexed as

Cell cycleGlioma stem cellsIFN-βImmune responseNeural stem cell

Identifiers

PMID35778531
PMCPMC9249963
OpenAlexW4283772160

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.