Evidence map›Paper›PMID 32452133›Full record

ArticleJournal of cellular and molecular medicine2020

MALT1 is a potential therapeutic target in glioblastoma and plays a crucial role in EGFR-induced NF-κB activation.

Xuejiao Liu, Chenglong Yue, Lin Shi, Guanzheng Liu, Qiyu Cao, Qianqian Shan, Yifeng Wang, Xiangyu Chen, Huan Li, Jie Wang and 3 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 32 citations in OpenAlex.

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  16. CORRIGENDUM.Journal of cellular and molecular medicine · 2022
    Article
  17. Article
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  19. Targeting MALT1 Suppresses the Malignant Progression of Colorectal CancerFrontiers in cell and developmental biology · 2022
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 1 institution in 1 country.

Xuejiao LiuInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.ORCID 0000-0001-8039-4174
Chenglong YueInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Lin ShiInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Guanzheng LiuInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Qiyu CaoInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Qianqian ShanInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Yifeng WangInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Xiangyu ChenInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Huan LiInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Jie WangInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Shangfeng GaoInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.ORCID 0000-0003-0340-2956
Mingshan NiuInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.
Rutong YuInsititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, China.ORCID 0000-0001-8533-1973
Xuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is the most common malignant tumour in the adult brain and hard to treat. Nuclear factor κB (NF-κB) signalling has a crucial role in the tumorigenesis of GBM. EGFR signalling is an important driver of NF-κB activation in GBM; however, the correlation between EGFR and the NF-κB pathway remains unclear. In this study, we investigated the role of mucosa-associated lymphoma antigen 1 (MALT1) in glioma progression and evaluated the anti-tumour activity and effectiveness of MI-2, a MALT1 inhibitor in a pre-clinical GBM model. We identified a paracaspase MALT1 that is involved in EGFR-induced NF-kB activation in GBM. MALT1 deficiency or inhibition significantly affected the proliferation, survival, migration and invasion of GBM cells both in vitro and in vivo. Moreover, MALT1 inhibition caused G1 cell cycle arrest by regulating multiple cell cycle-associated proteins. Mechanistically, MALTI inhibition blocks the degradation of IκBα and prevents the nuclear accumulation of the NF-κB p65 subunit in GBM cells. This study found that MALT1, a key signal transduction cascade, can mediate EGFR-induced NF-kB activation in GBM and may be potentially used as a novel therapeutic target for GBM.

Indexed as

Molecular Targeted TherapyAnimalsCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationEpidermal Growth FactorErbB ReceptorsGlioblastomaHumansMice, KnockoutMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNeoplasm InvasivenessNF-kappa BTumor Stem Cell AssayEpidermal Growth FactorErbB ReceptorsMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNF-kappa Bcell proliferationEGFR/ NF-κB signalling pathwayGBMMALT1MI-2

Identifiers

PMID32452133
PMCPMC7339184
OpenAlexW3032724680

What OpenQuestion holds

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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.