Evidence map›Paper›PMID 36512307›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2023

YBX1 regulates the survival of chronic myeloid leukemia stem cells by modulating m

Jihua Chai, Qifan Wang, Qiang Qiu, Guoqiang Han, Yilin Chen, Weiming Li, Haojian Zhang

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. NCellular and molecular life sciences : CMLS · 2024
    Review
  8. Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  9. Article
  10. Review
  11. Review
  12. Aberrant RNA mCell death & disease · 2023
    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

7 authors at 3 institutions in 1 country.

Jihua Chai *The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Medical Research Institute, Wuhan University, No.185, East Lake Road, Wuchang District, Wuhan, Hubei, 430071, People's Republic of China.
Qifan Wang *The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Medical Research Institute, Wuhan University, No.185, East Lake Road, Wuchang District, Wuhan, Hubei, 430071, People's Republic of China.
Qiang QiuState Key Laboratory of Biotherapy, West China Hospital & Collaborative Innovation Center for Biotherapy, Sichuan University, Chengdu, China.
Guoqiang HanFrontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan, China.
Yilin ChenDepartment of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Weiming LiDepartment of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Haojian ZhangThe State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Medical Research Institute, Wuhan University, No.185, East Lake Road, Wuchang District, Wuhan, Hubei, 430071, People's Republic of China. haojian_zhang@whu.edu.cn.
Wuhan University · CNHuazhong University of Science and Technology · CNState Key Laboratory of Biotherapy

Funding

National Natural Science Foundation of China 82230007
6 · The paper itself

Abstract

purposeChronic myeloid leukemia (CML) is a myeloproliferative disease derived from hematopoietic stem cells (HSCs) that harbor Philadelphia chromosome (Ph chromosome). In clinic, leukemia stem cells (LSCs) in CML are insensitive to the treatment with tyrosine kinase inhibitors, and are responsible for disease relapse. However, the molecular mechanisms for maintaining LSCs survival remain elusive.

methodsCML patient-derived cell lines and BCR-ABL-induced CML mouse model were used to explore the role of YBX1 in regulating the survival of CML LSCs. Bone marrow transduction and transplantation, and colony-forming unit assay were used to investigate LSC function. The underlying mechanism of how YBX1 regulates LSCs survival were assessed using flow cytometry, RNA sequencing, western blot, RNA decay assay, co-immunoprecipitation and RNA immunoprecipitation.

resultsHere we show that RNA-binding protein YBX1 plays an important role in regulating survival of CML LSCs. We find that YBX1 expression is significantly increased in CML cells, and confirm that YBX1 is required for maintaining survival of LSCs. Deletion of YBX1 impairs the propagation of CML through blocking cell proliferation and inducing apoptosis of LSCs. Mechanistically, we find that YBX1 regulates expression of apoptotic associated genes. YBX1 cooperates with RNA m

conclusionOur findings reveal a critical role of YBX1 in maintaining survival of CML LSCs, which provides a rationale for targeting YBX1 in CML treatment.

Indexed as

14-3-3 ProteinsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveNeoplastic Stem CellsAdenineAnimalsMiceRNATranscription Factors14-3-3 Proteins6-methyladenineAdenineRNATranscription FactorsYbx1 protein, mouseYwhaz protein, mouseChronic myeloid leukemiaLeukemia stem cellsRNA m6AYBX1YWHAZ

Identifiers

PMID36512307
PMCPMC12974669
OpenAlexW4311290989

What Socratic 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 Socratic graph.