Evidence map›Paper›PMID 29384529›Full record

ArticleBritish journal of cancer2018

Silencing of HMGA2 reverses retardance of cell differentiation in human myeloid leukaemia.

Li Tan, Hongfa Xu, Guoshu Chen, Xiaoping Wei, Baodan Yu, Jingmei Ye, Lihua Xu, Huo Tan

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Regulation of HSC development and function by Lin28b.Frontiers in cell and developmental biology · 2025
    Review
  4. Article
  5. Aberrant stem cell and developmental programs in pediatric leukemia.Frontiers in cell and developmental biology · 2024
    Review
  6. Complete miRNA-15/16 loss in mice promotes hematopoietic progenitor expansion and a myeloid-biased hyperproliferative state.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
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 3 institutions in 1 country.

Li TanDepartment of Hematology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510230, China.
Hongfa XuDepartment of Hematology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510230, China.
Guoshu ChenDepartment of Hematology, Huizhou Municipal Central Hospital, Huizhou 516001, China.
Xiaoping WeiClinical Laboratory, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China.
Baodan YuClinical Laboratory, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China.
Jingmei YeDepartment of Hematology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510230, China.
Lihua XuDepartment of Hematology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510230, China.
Huo TanDepartment of Hematology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510230, China.
First Affiliated Hospital of Guangzhou Medical University · CNGuangzhou Medical University · CNHuizhou Central People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHigh-mobility group AT-hook 2 (HMGA2) may serve as an architectural transcription factor, and it can regulate a range of normal biological processes including proliferation and differentiation. Upregulation of HMGA2 expression is correlated to the undifferentiated phenotype of immature leukaemic cells. However, the underlying mechanism of HMGA2-dependent myeloid differentiation blockage in leukaemia is unknown.

methodsTo reveal the role and mechanism of HMGA2 in differentiation arrest of myeloid leukaemia cells, the quantitative expression of HMGA2 and homeobox A9 (HOXA9) was analysed by real-time PCR (qRT-PCR). The regulatory function of HMGA2 in blockage of differentiation in human myeloid leukaemia was investigated through in vitro assays (XTT assay, May-Grünwald-Giemsa, flow cytometry analysis and western blot).

resultsWe found that the expression of HMGA2 and HOXA9 was reduced during the process of granulo-monocytic maturation of acute myeloid leukaemia (AML) cells, knockdown of HMGA2 promotes terminal (granulocytic and monocytic) differentiation of myeloid leukaemia primary blasts and cell lines, and HOXA9 was significantly downregulated in leukaemic cells with knockdown of HMGA2. Downregulation of HOXA9 in myeloid leukaemia cells led to increased differentiation capacity in vitro.

conclusionsOur data suggest that increased expression of HMGA2 represents a possible new mechanism of myeloid differentiation blockage of leukaemia. Aberrant expression of HMGA2 may enhance HOXA9-dependent leukaemogenesis and myeloid leukaemia phenotype. Disturbance of the HMGA2-HOXA9 pathway is probably a therapeutic strategy in myeloid leukaemia.

Indexed as

Antineoplastic AgentsCell DifferentiationCell ProliferationCell SurvivalDimethyl SulfoxideFree Radical ScavengersGene ExpressionGene Knockdown TechniquesGranulocytesHL-60 CellsHMGA2 ProteinHomeodomain ProteinsHumansK562 CellsLeukemia, Myeloid, AcuteMonocytesAntineoplastic AgentsDimethyl SulfoxideFree Radical ScavengersHMGA2 ProteinHMGA2 protein, humanhomeobox protein HOXA9Homeodomain ProteinsRNA, MessengerTretinoin

Identifiers

PMID29384529
PMCPMC5808023
OpenAlexW2782443054

What OpenQuestion holds

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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.