Evidence map›Paper›PMID 32661325›Full record

ArticleOncogene2020

Signal-transducing adapter protein-1 is required for maintenance of leukemic stem cells in CML.

Jun Toda, Michiko Ichii, Kenji Oritani, Hirohiko Shibayama, Akira Tanimura, Hideaki Saito, Takafumi Yokota, Daisuke Motooka, Daisuke Okuzaki, Yuichi Kitai and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2020. 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
1.8field-weighted citation impact, top 13% 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, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. SH2 Domains: Folding, Binding and Therapeutical Approaches.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Review
  10. 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

15 authors at 4 institutions in 1 country.

Jun TodaDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.ORCID http://orcid.org/0000-0002-0297-5640
Michiko IchiiDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan. michii@bldon.med.osaka-u.ac.jp.ORCID http://orcid.org/0000-0002-0018-6656
Kenji OritaniDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Hirohiko ShibayamaDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.ORCID http://orcid.org/0000-0003-4014-2815
Akira TanimuraDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Hideaki SaitoDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Takafumi YokotaDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Daisuke MotookaGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Daisuke OkuzakiGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.ORCID http://orcid.org/0000-0002-4552-783X
Yuichi KitaiDepartment of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.
Ryuta MuromotoDepartment of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.ORCID http://orcid.org/0000-0002-7474-493X
Jun-Ichi KashiwakuraDepartment of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.ORCID http://orcid.org/0000-0002-7863-6696
Tadashi MatsudaDepartment of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.
Naoki HosenDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
Yuzuru KanakuraDepartment of Hematology and Oncology, Osaka University Graduate School of Medicine, Suita, Japan.
The University of Osaka · JPHokkaido University · JPInternational University of Health and Welfare · JPSumitomo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The family of signal-transducing adapter proteins (STAPs) has been reported to be involved in a variety of intracellular signaling pathways and implicated as transcriptional factors. We previously cloned STAP-2 as a c-Fms interacting protein and explored its effects on chronic myeloid leukemia (CML) leukemogenesis. STAP-2 binds to BCR-ABL, upregulates BCR-ABL phosphorylation, and activates its downstream molecules. In this study, we evaluated the role of STAP-1, another member of the STAP family, in CML pathogenesis. We found that the expression of STAP-1 is aberrantly upregulated in CML stem cells (LSCs) in patients' bone marrow. Using experimental model mice, deletion of STAP-1 prolonged the survival of CML mice with inducing apoptosis of LSCs. The impaired phosphorylation status of STAT5 by STAP-1 ablation leads to downregulation of antiapoptotic genes, Bcl-2 and Bcl-xL. Interestingly, transcriptome analyses indicated that STAP-1 affects several signaling pathways related to BCR-ABL, JAK2, and PPARγ. This adapter protein directly binds to not only BCR-ABL, but also STAT5 proteins, showing synergistic effects of STAP-1 inhibition and BCR-ABL or JAK2 tyrosine kinase inhibition. Our results identified STAP-1 as a regulator of CML LSCs and suggested it to be a potential therapeutic target for CML.

Indexed as

Disease Models, AnimalGene Expression Regulation, LeukemicAdaptor Proteins, Signal TransducingAnimalsApoptosisCell Line, TumorFusion Proteins, bcr-ablGene Expression ProfilingHumansK562 CellsKaplan-Meier EstimateLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMice, Inbred C57BLMice, KnockoutNeoplastic Stem CellsProtein BindingAdaptor Proteins, Signal TransducingBCL2 protein, humanFusion Proteins, bcr-ablProto-Oncogene Proteins c-bcl-2STAP1 protein, humanSTAP-1 protein, mouse

Identifiers

PMID32661325
PMCPMC7441008
OpenAlexW3040886827

What OpenQuestion holds

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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.