Evidence map›Paper›PMID 21613208›Full record

ArticleThe Journal of biological chemistry2011

Insulin growth factor-2 binding protein 3 (IGF2BP3) is a glioblastoma-specific marker that activates phosphatidylinositol 3-kinase/mitogen-activated protein kinase (PI3K/MAPK) pathways by modulating IGF-2.

Ramaswamy Suvasini, Bhargava Shruti, Balaram Thota, Sridevi Vijay Shinde, Dinorah Friedmann-Morvinski, Zahid Nawaz, Krishnarao Venkatesh Prasanna, Kandavel Thennarasu, Alangar Sathyaranjandas Hegde, Arimappamagan Arivazhagan and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

107 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.

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47 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

13 authors at 4 institutions in 2 countries.

Ramaswamy SuvasiniDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore 560 012, India.
Bhargava Shruti
Balaram Thota
Sridevi Vijay Shinde
Dinorah Friedmann-Morvinski
Zahid Nawaz
Krishnarao Venkatesh Prasanna
Kandavel Thennarasu
Alangar Sathyaranjandas Hegde
Arimappamagan Arivazhagan
Bangalore Ashwathnarayanarao Chandramouli
Vani Santosh
Kumaravel Somasundaram
Indian Institute of Science Bangalore · INNational Institute of Mental Health and Neurosciences · INSri Sathya Sai Institute of Higher Medical Sciences · INSalk Institute for Biological Studies · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma is the most common and malignant form of primary astrocytoma. Upon investigation of the insulin-like growth factor (IGF) pathway, we found the IGF2BP3/IMP3 transcript and protein to be up-regulated in GBMs but not in lower grade astrocytomas (p < 0.0001). IMP3 is an RNA binding protein known to bind to the 5'-untranslated region of IGF-2 mRNA, thereby activating its translation. Overexpression- and knockdown-based studies establish a role for IMP3 in promoting proliferation, anchorage-independent growth, invasion, and chemoresistance. IMP3 overexpressing B16F10 cells also showed increased tumor growth, angiogenesis, and metastasis, resulting in poor survival in a mouse model. Additionally, the infiltrating front, perivascular, and subpial regions in a majority of the GBMs stained positive for IMP3. Furthermore, two different murine glioma models were used to substantiate the above findings. In agreement with the translation activation functions of IMP3, we also found increased IGF-2 protein in the GBM tumor samples without a corresponding increase in its transcript levels. Also, in vitro IMP3 overexpression/knockdown modulated the IGF-2 protein levels without altering its transcript levels. Additionally, IGF-2 neutralization and supplementation studies established that the proproliferative effects of IMP3 were indeed mediated through IGF-2. Concordantly, PI3K and MAPK, the downstream effectors of IGF-2, are activated by IMP3 and are found to be essential for IMP3-induced cell proliferation. Thus, we have identified IMP3 as a GBM-specific proproliferative and proinvasive marker acting through IGF-2 resulting in the activation of oncogenic PI3K and MAPK pathways.

Indexed as

MAP Kinase Signaling SystemAdolescentAdultAgedAnimalsBiomarkers, TumorCell Line, TumorCell ProliferationDrug Resistance, NeoplasmGlioblastomaHumansInsulin-Like Growth Factor IIMiceMiddle AgedMitogen-Activated Protein KinasesNeoplasm InvasivenessBiomarkers, TumorIGF2BP3 protein, humanInsulin-Like Growth Factor IIMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID21613208
PMCPMC3138258
OpenAlexW2061224512

What OpenQuestion holds

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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.