Evidence map›Paper›PMID 25737450›Full record

ArticleThe Journal of biological chemistry2015

Knockdown of SALL4 Protein Enhances All-trans Retinoic Acid-induced Cellular Differentiation in Acute Myeloid Leukemia Cells.

Li Liu, Liang Liu, Lai-Han Leung, Austin J Cooney, Changyi Chen, Todd K Rosengart, Yupo Ma, Jianchang Yang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Functional and clinical significance of SALL4 in breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  13. 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 4 institutions in 2 countries.

Li LiuFrom the Departments of Surgery and.
Liang Liuthe Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology, Macau 519020, China, and.
Lai-Han Leungthe Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology, Macau 519020, China, and.
Austin J Cooneythe Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas 77030.
Changyi Chenthe Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas 77030.
Todd K Rosengartthe Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas 77030.
Yupo MaPathology, State University of New York at Stony Brook, Stony Brook, New York 11794.
Jianchang YangFrom the Departments of Surgery and Pathology, State University of New York at Stony Brook, Stony Brook, New York 11794, jianchang.yang@bcm.edu.
Baylor College of Medicine · USMacau University of Science and Technology · MOState University of New York · USStony Brook University · US

Funding

In Situ Cardiac Infarct Cellular ReprogrammingR01HL121294 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI ROSENGART, TODD K · 2015 to 2018
$2.7M
NHLBI NIH HHS R01 HL121294
6 · The paper itself

Abstract

All-trans retinoic acid (ATRA) is a differentiation agent that revolutionized the treatment of acute promyelocytic leukemia. However, it has not been useful for other types of acute myeloid leukemia (AML). Here we explored the effect of SALL4, a stem cell factor, on ATRA-induced AML differentiation in both ATRA-sensitive and ATRA-resistant AML cells. Aberrant SALL4 expression has been found in nearly all human AML cases, whereas, in normal bone marrow and peripheral blood cells, its expression is only restricted to hematopoietic stem/progenitor cells. We reason that, in AMLs, SALL4 activation may prevent cell differentiation and/or protect self-renewal that is seen in normal hematopoietic stem/progenitor cells. Indeed, our studies show that ATRA-mediated myeloid differentiation can be largely blocked by exogenous expression of SALL4, whereas ATRA plus SALL4 knockdown causes significantly increased AML differentiation and cell death. Mechanistic studies indicate that SALL4 directly associates with retinoic acid receptor α and modulates ATRA target gene expression. SALL4 is shown to recruit lysine-specific histone demethylase 1 (LSD1) to target genes and alter the histone methylation status. Furthermore, coinhibition of LSD1 and SALL4 plus ATRA treatment exhibited the strongest anti-AML effect. These findings suggest that SALL4 plays an unfavorable role in ATRA-based regimes, highlighting an important aspect of leukemia therapy.

Indexed as

AnimalsAntineoplastic AgentsCell DifferentiationCell Line, TumorFemaleGene Knockdown TechniquesHematopoietic Stem CellsHistone DemethylasesHL-60 CellsHumansLeukemia, Myeloid, AcuteMiceMice, Inbred NODMice, SCIDNeoplastic Stem CellsReceptors, Retinoic AcidAntineoplastic AgentsHistone DemethylasesKDM1A protein, humanRARA protein, humanRara protein, mouseReceptors, Retinoic AcidRetinoic Acid Receptor alphaRNA, Small InterferingSALL4 protein, humanTranscription FactorsTretinoinHematopoietic Stem CellsHistone DemethylaseStem CellsTranscription CorepressorTumor Therapy

Identifiers

PMID25737450
PMCPMC4409227
OpenAlexW2015154759

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.