Evidence map›Paper›PMID 34042961›Full record

ArticleNeuro-oncology2021

Spliceosome-regulated RSRP1-dependent NF-κB activation promotes the glioblastoma mesenchymal phenotype.

Yaomin Li, Xiran Wang, Songtao Qi, Lei Gao, Guanglong Huang, Zhonglu Ren, Kaishu Li, Yuping Peng, Guozhong Yi, Jinglin Guo and 4 more

Open access · greenAbstract read
In one paragraph

Article in Neuro-oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 47 citations in OpenAlex.

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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 2 institutions in 1 country.

Yaomin LiDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Xiran WangDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Songtao QiDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID 0000-0001-7600-9528
Lei GaoDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Guanglong HuangDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Zhonglu RenCollege of Medical Information Engineering, Guangdong Pharmaceutical University, Guangzhou, Guangdong, China.
Kaishu LiDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Yuping PengDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Guozhong YiDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Jinglin GuoDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Runwei YangDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Hai WangDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Xian ZhangDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Yawei LiuDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID 0000-0003-4535-5019
Nanfang Hospital · CNGuangdong Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe glioblastoma (GBM) mesenchymal (MES) phenotype, induced by NF-κB activation, is characterized by aggressive tumor progression and poor clinical outcomes. Our previous analysis indicated that MES GBM has a unique alternative splicing (AS) pattern; however, the underlying mechanism remains obscure. We aimed to reveal how splicing regulation contributes to MES phenotype promotion in GBM.

methodsWe screened novel candidate splicing factors that participate in NF-κB activation and MES phenotype promotion in GBM. In vitro and in vivo assays were used to explore the function of RSRP1 in MES GBM.

resultsHere, we identified that arginine/serine-rich protein 1 (RSRP1) promotes the MES phenotype by facilitating GBM cell invasion and apoptosis resistance. Proteomic, transcriptomic, and functional analyses confirmed that RSRP1 regulates AS in MES GBM through mediating spliceosome assembly. One RSRP1-regulated AS event resulted in skipping PARP6 exon 18 to form truncated, oncogenic PARP6-s. This isoform was unable to effectively suppress NF-κB. Cotreatment of cultured GBM cells and GBM tumor-bearing mice with spliceosome and NF-κB inhibitors exerted a synergistic effect on MES GBM growth.

conclusionWe identified a novel mechanism through which RSRP1-dependent splicing promotes the GBM MES phenotype. Targeting AS via RSRP1-related spliceosomal factors might constitute a promising treatment for GBM.

Indexed as

Brain NeoplasmsGlioblastomaAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticMiceNeoplasm ProteinsNF-kappa BPhenotypeProteomicsSpliceosomesNeoplasm ProteinsNF-kappa Bglioblastomamesenchymal phenotypeNF-κBRSRP1spliceosome

Identifiers

PMID34042961
PMCPMC8485435
OpenAlexW3164692546

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.