Evidence map›Paper›PMID 32926734›Full record

ArticleNeuro-oncology2021

EIF4A3-induced circular RNA ASAP1 promotes tumorigenesis and temozolomide resistance of glioblastoma via NRAS/MEK1/ERK1-2 signaling.

Yutian Wei, Chenfei Lu, Peng Zhou, Lin Zhao, Xiao Lyu, Jianxing Yin, ZhuMei Shi, Yongping You

Open access · hybridAbstract 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 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
17.6field-weighted citation impact, top 1% 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

137 citing papers in PubMed, 295 citations in OpenAlex.

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  9. Recent advances in molecular mechanisms of microRNAs in pathogenesis and resistance of treatment in glioblastoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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77 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Yutian WeiDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Chenfei LuDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Peng ZhouDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Lin ZhaoDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Xiao LyuDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jianxing YinDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
ZhuMei ShiDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yongping YouDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Nanjing Medical University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcquired chemoresistance is a major challenge in the clinical treatment of glioblastoma (GBM). Circular RNAs have been verified to play a role in tumor chemoresistance. However, the underlying mechanisms remain unclear. The aim of this study was to elucidate the potential role and molecular mechanism of circular (circ)RNA ADP-ribosylation factor GTPase activating proteins with Src homology 3 domain, ankyrin repeat and Pleckstrin homology domain 1 (circASAP1) in temozolomide (TMZ) resistance of GBM.

methodsWe analyzed circRNA alterations in recurrent GBM tissues relative to primary GBM through RNA sequencing. Real-time quantitative reverse transcription PCR verified the expression of circASAP1 in tissues and cells. Knockdown and overexpressed plasmids were used to evaluate the effect of circASAP1 on GBM cell proliferation and TMZ-induced apoptosis. Mechanistically, fluorescent in situ hybridization, dual-luciferase reporter, and RNA immunoprecipitation assays were performed to confirm the regulatory network of circASAP1/miR-502-5p/neuroblastoma Ras (NRAS). An intracranial tumor model was used to verify our findings in vivo.

resultsCircASAP1 expression was significantly upregulated in recurrent GBM tissues and TMZ-resistant cell lines. CircASAP1 overexpression enhanced GBM cell proliferation and TMZ resistance, which could be reduced by circASAP1 knockdown. Further experiments revealed that circASAP1 increased the expression of NRAS via sponging miR-502-5p. Moreover, circASAP1 depletion effectively restored the sensitivity of TMZ-resistant xenografts to TMZ treatment in vivo.

conclusionsOur data demonstrate that circASAP1 exerts regulatory functions in GBM and that competing endogenous (ce)RNA-mediated microRNA sequestration might be a potential therapeutic strategy for GBM treatment.

Indexed as

Brain NeoplasmsGlioblastomaMicroRNAsNeuroblastomaAdaptor Proteins, Signal TransducingCarcinogenesisCell Line, TumorCell ProliferationDEAD-box RNA HelicasesDrug Resistance, NeoplasmEukaryotic Initiation Factor-4AGene Expression Regulation, NeoplasticGTP PhosphohydrolasesHumansIn Situ Hybridization, FluorescenceMembrane ProteinsAdaptor Proteins, Signal TransducingASAP1 protein, humanDEAD-box RNA HelicasesEIF4A3 protein, humanEukaryotic Initiation Factor-4AGTP PhosphohydrolasesMembrane ProteinsMicroRNAsNRAS protein, humanRNA, CircularTemozolomidecircASAP1glioblastomamiR-502-5pNRAStemozolomide resistance

Identifiers

PMID32926734
PMCPMC8041353
OpenAlexW3085127652

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.