Evidence map›Paper›PMID 37157016›Full record

ArticleLeukemia2023

A novel lncRNA SNHG29 regulates EP300- related histone acetylation modification and inhibits FLT3-ITD AML development.

Shan Liu, Jie Zhou, Xiangling Ye, Danni Chen, Weimin Chen, Yaobin Lin, Zhizhong Chen, Biyun Chen, Jin Shang

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. LncRNAiScience · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Epigenomics · 2024
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 2 countries.

Shan LiuDepartment of Hematology-Oncology, Fujian Children's Hospital; College of Clinical Medicine for Obstetrics and Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China.
Jie ZhouShengli Clinical Medical College of Fujian Medical University; Department of Hematology, Fujian Provincial Hospital, Fuzhou, Fujian, China.
Xiangling YeShengli Clinical Medical College of Fujian Medical University; Department of Hematology, Fujian Provincial Hospital, Fuzhou, Fujian, China.
Danni ChenShengli Clinical Medical College of Fujian Medical University; Department of Hematology, Fujian Provincial Hospital, Fuzhou, Fujian, China.
Weimin ChenShengli Clinical Medical College of Fujian Medical University; Department of Hematology, Fujian Provincial Hospital, Fuzhou, Fujian, China.
Yaobin LinClinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, Fujian, China.
Zhizhong ChenShengli Clinical Medical College of Fujian Medical University; Department of Pathology, Fujian Provincial Hospital, Fuzhou, Fujian, China.
Biyun ChenShengli Clinical Medical College of Fujian Medical University; Department of Hematology, Fujian Provincial Hospital, Fuzhou, Fujian, China.
Jin ShangShengli Clinical Medical College of Fujian Medical University; Department of Hematology, Fujian Provincial Hospital, Fuzhou, Fujian, China. dukepck@163.com.ORCID http://orcid.org/0000-0002-9122-3298
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Internal tandem duplication (ITD) mutations within the FMS-like tyrosine kinase-3 (FLT3) occur in up to 25% of acute myeloid leukemia (AML) patients and indicate a very poor prognosis. The role of long noncoding RNAs (lncRNAs) in FLT3-ITD AML progression remains unexplored. We identified a novel lncRNA, SNHG29, whose expression is specifically regulated by the FLT3-STAT5 signaling pathway and is abnormally down-regulated in FLT3-ITD AML cell lines. SNHG29 functions as a tumor suppressor, significantly inhibiting FLT3-ITD AML cell proliferation and decreasing sensitivity to cytarabine in vitro and in vivo models. Mechanistically, we demonstrated that SNHG29's molecular mechanism is EP300-binding dependent and identified the EP300-interacting region of SNHG29. SNHG29 modulates genome-wide EP300 genomic binding, affecting EP300-mediated histone modification and consequently influencing the expression of varies downstream AML-associated genes. Our study uncovers a novel molecular mechanism for SNHG29 in mediating FLT3-ITD AML biological behaviors through epigenetic modification, suggesting that SNHG29 could be a potential therapeutic target for FLT3-ITD AML.

Indexed as

Leukemia, Myeloid, AcuteRNA, Long NoncodingAcetylationE1A-Associated p300 Proteinfms-Like Tyrosine Kinase 3HistonesHumansMutationE1A-Associated p300 ProteinEP300 protein, humanFLT3 protein, humanfms-Like Tyrosine Kinase 3HistonesRNA, Long Noncoding

Identifiers

PMID37157016
OpenAlexW4375861126

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.