Evidence map›Paper›PMID 28465487›Full record

ArticleOncotarget2017

IGF2 mRNA binding protein 3 (IMP3) promotes glioma cell migration by enhancing the translation of RELA/p65.

Shruti Bhargava, Abhirami Visvanathan, Vikas Patil, Anuj Kumar, Santosh Kesari, Saumitra Das, Alangar S Hegde, Arimappamagan Arivazhagan, Vani Santosh, Kumaravel Somasundaram

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

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  15. Identification of Critical mBioMed research international · 2021
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  16. m6A modification in RNA: biogenesis, functions and roles in gliomas.Journal of experimental & clinical cancer research : CR · 2020
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  17. Insights into the Regulatory Role of mInternational journal of molecular sciences · 2020
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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

10 authors at 4 institutions in 2 countries.

Shruti BhargavaDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.
Abhirami VisvanathanDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.
Vikas PatilDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.
Anuj KumarDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.
Santosh KesariDepartment of Translational Neuro-Oncology and Neurotherapeutics, Pacific Neuroscience Institute, John Wayne Cancer Institute, Providence Saint John's Health Center, Santa Monica, California, USA.
Saumitra DasDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.
Alangar S HegdeSri Satya Sai Institute of Higher Medical Sciences, Bangalore, India.
Arimappamagan ArivazhaganDepartments of Neurosurgery, National Institute of Mental Health and Neuro Sciences, Bangalore, India.
Vani SantoshDepartments of Neuropathology, National Institute of Mental Health and Neuro Sciences, Bangalore, India.
Kumaravel SomasundaramDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.
Indian Institute of Science Bangalore · INNational Institute of Mental Health and Neurosciences · INSaint John's Health Center · USSri Sathya Sai Institute of Higher Medical Sciences · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The diffusely infiltrative nature of glioblastoma (GBM) makes them highly recurrent. IGF2 mRNA-binding protein 3 (IMP3), a GBM upregulated RNA binding protein, promotes glioma cell migration. An integrative bioinformatics analysis identified p65 (RELA), a subunit of NF-κB heterodimer as a target and an important mediator of IMP3 promoted glioma cell migration. IMP3 increased p65 protein levels without any change in p65 transcript levels, but promoted its polysome association. RIP-PCR demonstrated the binding of IMP3 to p65 transcript. UV crosslinking experiments with in vitro transcribed RNA confirmed the specific and direct binding of IMP3 to sites on p65 3'UTR. Further, IMP3 induced luciferase activity from p65 3'UTR reporter carrying wild type sites but not mutated sites. Exogenous overexpression of p65 from a 3'UTR-less construct rescued the reduced migration of glioma cells in IMP3 silenced condition. In addition, IMP3 silencing inhibited glioma stem-like cell maintenance and migration. The exogenous overexpression of 3'UTR-less p65 significantly alleviated the inhibition of neurosphere formation observed in IMP3 silenced glioma stem-like cells. Further, we show that IMP3 is transcriptionally activated by NF-κB pathway indicating the presence of a positive feedback loop between IMP3 and p65. This study establishes p65 as a novel target of IMP3 in increasing glioma cell migration and underscores the significance of IMP3-p65 feedback loop for therapeutic targeting in GBM.

Indexed as

3' Untranslated RegionsCell MovementGene Expression Regulation, NeoplasticGlioblastomaHCT116 CellsHEK293 CellsHumansRNA-Binding ProteinsSpheroids, CellularTranscriptional ActivationTranscription Factor RelATumor Cells, Cultured3' Untranslated RegionsIGF2BP3 protein, humanRELA protein, humanRNA-Binding ProteinsTranscription Factor RelAIMP3NF-κB signallingRELA/p65RNA binding proteintranslation control

Identifiers

PMID28465487
PMCPMC5522290
OpenAlexW2606742643

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.