Evidence map›Paper›PMID 25053419›Full record

ArticleThe Journal of biological chemistry2014

GSK3 protein positively regulates type I insulin-like growth factor receptor through forkhead transcription factors FOXO1/3/4.

Xiaodong Huo, Shu Liu, Ting Shao, Hui Hua, Qingbin Kong, Jiao Wang, Ting Luo, Yangfu Jiang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Non-microglial downregulation ofbioRxiv : the preprint server for biology · 2026
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  7. Targeting Akt in cancer for precision therapy.Journal of hematology & oncology · 2021
    Review
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  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Regulation of FOXO Factors in Mammalian Cells.Current topics in developmental biology · 2018
    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

8 authors at 2 institutions in 1 country.

Xiaodong HuoFrom the State Key Laboratory of Biotherapy, Section of Oncogene, West China Hospital, Sichuan University, Chengdu 610041.
Shu LiuFrom the State Key Laboratory of Biotherapy, Section of Oncogene, West China Hospital, Sichuan University, Chengdu 610041.
Ting ShaoFrom the State Key Laboratory of Biotherapy, Section of Oncogene, West China Hospital, Sichuan University, Chengdu 610041.
Hui Huathe Laboratory of Stem Cell Biology, West China Hospital, Chengdu 610041.
Qingbin KongFrom the State Key Laboratory of Biotherapy, Section of Oncogene, West China Hospital, Sichuan University, Chengdu 610041.
Jiao Wangthe School of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 610075, and.
Ting Luothe Cancer Center, West China Hospital, Chengdu 610041, China.
Yangfu JiangFrom the State Key Laboratory of Biotherapy, Section of Oncogene, West China Hospital, Sichuan University, Chengdu 610041, jyangfu@scu.edu.cn.
Chengdu University of Traditional Chinese Medicine · CNSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycogen synthase kinase-3 (GSK3) has either tumor-suppressive roles or pro-tumor roles in different types of human tumors. A number of GSK3 targets in diverse signaling pathways have been uncovered, such as tuberous sclerosis complex subunit 2 and β-catenin. The O subfamily of forkhead/winged helix transcription factors (FOXO) is known as tumor suppressors that induce apoptosis. In this study, we find that FOXO binds to type I insulin-like growth factor receptor (IGF-IR) promoter and stimulates its transcription. GSK3 positively regulates the transactivation activity of FOXO and stimulates IGF-IR expression. Although kinase-dead GSK3β cannot up-regulate IGF-IR, the constitutively active GSK3β induces IGF-IR expression in a FOXO-dependent manner. Serum starvation or Akt inhibition leads to an increase in IGF-IR expression, which could be blunted by GSK3 inhibition. GSK3β knockdown or GSK3 inhibitor suppresses IGF-I-induced IGF-IR, Akt, and ERK1/2 phosphorylation. Moreover, knockdown of GSK3β or FOXO1/3/4 leads to a decrease in cellular proliferation and abrogates IGF-I-induced hepatoma cell proliferation. These results suggest that GSK3 and FOXO may positively regulate IGF-I signaling and hepatoma cell proliferation.

Indexed as

Blotting, WesternCell Cycle ProteinsCell Line, TumorCell ProliferationExtracellular Signal-Regulated MAP KinasesForkhead Box Protein O1Forkhead Box Protein O3Forkhead Transcription FactorsGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansInsulin-Like Growth Factor IModels, GeneticPhosphorylationPromoter Regions, GeneticCell Cycle ProteinsExtracellular Signal-Regulated MAP KinasesForkhead Box Protein O1Forkhead Box Protein O3Forkhead Transcription FactorsFOXO1 protein, humanFOXO3 protein, humanFOXO4 protein, humanGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanInsulin-Like Growth Factor IProto-Oncogene Proteins c-aktReceptor, IGF Type 1Transcription FactorsCancerFOXOGlycogen Synthase Kinase 3 (GSK-3)Insulin-like Growth Factor (IGF)Receptor Tyrosine Kinase

Identifiers

PMID25053419
PMCPMC4155645
OpenAlexW2065759966

What OpenQuestion holds

Textmetadata
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.