Evidence map›Paper›PMID 29307582›Full record

ArticleStem cell reports2018

IGF-1R Promotes Symmetric Self-Renewal and Migration of Alkaline Phosphatase

Yung-Che Kuo, Heng-Kien Au, Jue-Liang Hsu, Hsiao-Feng Wang, Chiung-Ju Lee, Syue-Wei Peng, Ssu-Chuan Lai, Yu-Chih Wu, Hong-Nerng Ho, Yen-Hua Huang

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.5field-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

20 citing papers in PubMed, 34 citations in OpenAlex.

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  14. SOD2 acetylation on lysine 68 promotes stem cell reprogramming in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2019
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  19. TWEAK regulates the functions of hair follicle stem cells via the Fn14-Wnt/β-catenin-CXCR4 signalling axis.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
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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 1 country.

Yung-Che KuoDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, 11031 Taipei, Taiwan; Center for Cell Therapy and Regeneration Medicine, Taipei Medical University, 11031 Taipei, Taiwan.
Heng-Kien AuDepartment of Obstetrics and Gynecology, School of Medicine, College of Medicine, Taipei Medical University, 11031 Taipei, Taiwan; Center for Reproductive Medicine, Taipei Medical University Hospital, Taipei Medical University, 11031 Taipei, Taiwan; Department of Obstetrics and Gynecology, Taipei Medical University Hospital, 11031 Taipei, Taiwan.
Jue-Liang HsuDepartment of Biological Science and Technology, National Pingtung University of Science and Technology, 91201 Pingtung, Taiwan.
Hsiao-Feng WangDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, 11031 Taipei, Taiwan; Center for Cell Therapy and Regeneration Medicine, Taipei Medical University, 11031 Taipei, Taiwan.
Chiung-Ju LeeDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, 11031 Taipei, Taiwan; Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, 11031 Taipei, Taiwan.
Syue-Wei PengDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, 11031 Taipei, Taiwan; Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, 11031 Taipei, Taiwan.
Ssu-Chuan LaiDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, 11031 Taipei, Taiwan; Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, 11031 Taipei, Taiwan.
Yu-Chih WuCenter for Cell Therapy and Regeneration Medicine, Taipei Medical University, 11031 Taipei, Taiwan.
Hong-Nerng HoGraduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, 10002 Taipei, Taiwan; Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology and Infertility, National Taiwan University and Hospital, 10041 Taipei, Taiwan.
Yen-Hua HuangDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, 11031 Taipei, Taiwan; International PhD Program for Cell Therapy and Regeneration Medicine, College of Medicine, Taipei Medical University, 11031 Taipei, Taiwan; Center for Cell Therapy and Regeneration Medicine, Taipei Medical University, 11031 Taipei, Taiwan; Center for Reproductive Medicine, Taipei Medical University Hospital, Taipei Medical University, 11031 Taipei, Taiwan; Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, 11031 Taipei, Taiwan; Comprehensive Cancer Center of Taipei Medical University, 10031 Taipei, Taiwan; The Ph.D. Program for Translational Medicine, College of Medical Science and Technology, Taipei Medical University, 10031 Taipei, Taiwan. Electronic address: rita1204@tmu.edu.tw.
Taipei Medical University · TWNational Pingtung University of Science and Technology · TWNational Taiwan University · TWTaipei Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia cooperates with endocrine signaling to maintain the symmetric self-renewal proliferation and migration of embryonic germline stem cells (GSCs). However, the lack of an appropriate in vitro cell model has dramatically hindered the understanding of the mechanism underlying this cooperation. Here, using a serum-free system, we demonstrated that hypoxia significantly induced the GSC mesenchymal transition, increased the expression levels of the pluripotent transcription factor OCT4 and migration-associated proteins (SDF-1, CXCR4, IGF-1, and IGF-1R), and activated the cellular expression and translocalization of the CXCR4-downstream proteins ARP3/pFAK. The underlying mechanism involved significant IGF-1/IGF-1R activation of OCT4/CXCR4 expression through HIF-2α regulation. Picropodophyllin-induced inhibition of IGF-1R phosphorylation significantly suppressed hypoxia-induced SDF-1/CXCR4 expression and cell migration. Furthermore, transactivation between IGF-1R and CXCR4 was involved. In summary, we demonstrated that niche hypoxia synergistically cooperates with its associated IGF-1R signaling to regulate the symmetric division (self-renewal proliferation) and cell migration of alkaline phosphatase-positive GSCs through HIF-2α-OCT4/CXCR4 during embryogenesis.

Indexed as

AnimalsCell HypoxiaCell MovementCell ProliferationCell Self RenewalChemokine CXCL12Embryonic Germ CellsGene Expression Regulation, DevelopmentalMiceOctamer Transcription Factor-3PhosphorylationReceptor, IGF Type 1Receptors, CXCR4Signal TransductionStem Cell NicheTranscription FactorsChemokine CXCL12CXCR4 protein, mouseHIF-2 protein, mouseOctamer Transcription Factor-3Pou5f1 protein, mouseReceptor, IGF Type 1Receptors, CXCR4Transcription FactorsCXCR4germline stem cellsHIF-2αhypoxiaIGF-1RmigrationnicheOCT4SDF-1self-renewal

Identifiers

PMID29307582
PMCPMC5830933
OpenAlexW2782494469

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.