Evidence map›Paper›PMID 37298628›Full record

ArticleInternational journal of molecular sciences2023

IGFBP7 Fuels the Glycolytic Metabolism in B-Cell Precursor Acute Lymphoblastic Leukemia by Sustaining Activation of the IGF1R-Akt-GLUT1 Axis.

Leonardo Luís Artico, Juliana Silveira Ruas, José Ricardo Teixeira Júnior, Natacha Azussa Migita, Gustavo Seguchi, Xinghua Shi, Silvia Regina Brandalise, Roger Frigério Castilho, José Andrés Yunes

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. A guide to B cell metabolism.Nature reviews. Immunology · 2026
    Review
  2. Article
  3. Article
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  9. Review
  10. The multifaceted role of insulin-like growth factor binding protein 7.Frontiers in cell and developmental biology · 2024
    Review
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

9 authors at 3 institutions in 2 countries.

Leonardo Luís ArticoCentro Infantil Boldrini, Campinas 13083-210, SP, Brazil.
Juliana Silveira RuasCentro Infantil Boldrini, Campinas 13083-210, SP, Brazil.ORCID 0000-0002-5967-5235
José Ricardo Teixeira JúniorCentro Infantil Boldrini, Campinas 13083-210, SP, Brazil.ORCID 0000-0003-3704-7649
Natacha Azussa MigitaCentro Infantil Boldrini, Campinas 13083-210, SP, Brazil.ORCID 0000-0002-1326-3841
Gustavo SeguchiCentro Infantil Boldrini, Campinas 13083-210, SP, Brazil.ORCID 0000-0001-7078-1162
Xinghua ShiDepartment of Computer and Information Sciences, Temple University, Philadelphia, PA 19122, USA.
Silvia Regina BrandaliseCentro Infantil Boldrini, Campinas 13083-210, SP, Brazil.
Roger Frigério CastilhoDepartment of Pathology, School of Medical Sciences, University of Campinas, Campinas 13083-887, SP, Brazil.ORCID 0000-0003-2338-8717
José Andrés YunesCentro Infantil Boldrini, Campinas 13083-210, SP, Brazil.ORCID 0000-0002-1316-3525
Centro Infantil Boldrini · BRUniversidade Estadual de Campinas (UNICAMP) · BRTemple University · US

Funding

National Council for Scientific and Technological Development 301596/2017-4National Council for Scientific and Technological Development 305896/2013-0National Council for Scientific and Technological Development 308399/2021-8National Council for Scientific and Technological Development 471003/2013-1São Paulo Research Foundation 12/12802-1São Paulo Research Foundation 14/20015-5São Paulo Research Foundation 17/17728-8São Paulo Research Foundation 2019/04943-3São Paulo Research Foundation 2022/04464-0
6 · The paper itself

Abstract

Increased glycolytic metabolism plays an important role in B-cell precursor Acute Lymphoblastic Leukemia (BCP-ALL). We previously showed that IGFBP7 exerts mitogenic and prosuvival effects in ALL by promoting IGF1 receptor (IGF1R) permanence on the cell surface, thus prolonging Akt activation upon IGFs/insulin stimulation. Here, we show that sustained activation of the IGF1R-PI3K-Akt axis concurs with GLUT1 upregulation, which enhances energy metabolism and increases glycolytic metabolism in BCP-ALL. IGFBP7 neutralization with a monoclonal antibody or the pharmacological inhibition of the PI3K-Akt pathway was shown to abrogate this effect, restoring the physiological levels of GLUT1 on the cell surface. The metabolic effect described here may offer an additional mechanistic explanation for the strong negative impact seen in ALL cells in vitro and in vivo after the knockdown or antibody neutralization of IGFBP7, while reinforcing the notion that it is a valid target for future therapeutic interventions.

Indexed as

Insulin-Like Growth Factor Binding ProteinsPrecursor B-Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene Proteins c-aktCell Line, TumorCell ProliferationGlucose Transporter Type 1HumansPhosphatidylinositol 3-KinasesReceptor, IGF Type 1Glucose Transporter Type 1IGF1R protein, humaninsulin-like growth factor binding protein-related protein 1Insulin-Like Growth Factor Binding ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, IGF Type 1Acute Lymphoblastic LeukemiaGLUT1IGF1RIGFBP7PI3K–Akt

Identifiers

PMID37298628
PMCPMC10253689
OpenAlexW4379141697

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.