Evidence map›Paper›PMID 28107692›Full record

ArticleLeukemia research2017

RNA binding protein MSI2 positively regulates FLT3 expression in myeloid leukemia.

Ayuna Hattori, Daniel McSkimming, Natarajan Kannan, Takahiro Ito

Open access · greenAbstract read
In one paragraph

Article in Leukemia research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 32% 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, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. RNA Regulators in Leukemia and Lymphoma.Cold Spring Harbor perspectives in medicine · 2020
    Review
  12. Deciphering Key Pharmacological Pathways of Qingdai Acting on Chronic Myeloid Leukemia Using a Network Pharmacology-Based Strategy.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  13. Article
  14. FLT3-ITD and its current role in acute myeloid leukaemia.Medical oncology (Northwood, London, England) · 2017
    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

4 authors at 2 institutions in 1 country.

Ayuna HattoriDepartment of Biochemistry and Molecular Biology, Franklin College of Arts and Sciences, and UGA Cancer Center, The University of Georgia, Athens, GA 30602, United States.
Daniel McSkimmingDepartment of Biochemistry and Molecular Biology, Franklin College of Arts and Sciences, and UGA Cancer Center, The University of Georgia, Athens, GA 30602, United States.
Natarajan KannanDepartment of Biochemistry and Molecular Biology, Franklin College of Arts and Sciences, and UGA Cancer Center, The University of Georgia, Athens, GA 30602, United States.
Takahiro ItoDepartment of Biochemistry and Molecular Biology, Franklin College of Arts and Sciences, and UGA Cancer Center, The University of Georgia, Athens, GA 30602, United States. Electronic address: ito@bmb.uga.edu.
University of Georgia · USFranklin College · US

Funding

Functional Annotation of Natural and Disease Variants in Tryosine KinasesR01GM114409 · NIGMS · UNIVERSITY OF GEORGIA · PI KANNAN, NATARAJAN · 2015 to 2020
$1.6M
NIGMS NIH HHS R01 GM114409
6 · The paper itself

Abstract

FLT3 is frequently mutated and overexpressed in acute myelogenous leukemia (AML) and other hematologic malignancies. Although signaling events downstream of FLT3 receptor tyrosine kinase have been studied in depth, molecular mechanisms of how FLT3 expression is regulated at the post-transcriptional level in particular remain elusive. In this study, we investigated the roles of an RNA binding protein MSI2 as a regulator of FLT3 expression. MSI2 and FLT3 are significantly co-regulated in human AML and chronic myelogenous leukemia in blast crisis (BC-CML). Genetic loss of MSI2 leads to down-regulation of the FLT3 receptor in both AML and BC-CML cells and concomitant impairment of clonogenic growth potential. Furthermore, we demonstrate that MSI2 protein is physically bound to FLT3 mRNA transcripts, suggesting post-transcriptional control of FLT3 expression. Collectively, these results reveal a novel mode of FLT3 regulation essential for leukemia growth, which may aid in designing a targeted therapy to treat human myeloid leukemia.

Indexed as

AnimalsCell Line, TumorDown-Regulationfms-Like Tyrosine Kinase 3Gene Expression Regulation, NeoplasticHumansLeukemia, Myeloid, AcuteMiceRNA-Binding ProteinsFLT3 protein, humanfms-Like Tyrosine Kinase 3MSI2 protein, humanRNA-Binding ProteinsAcute myelogenous leukemiaChronic myelogenous leukemiaFLT3Post-transcriptional regulationRNA binding proteins

Identifiers

PMID28107692
PMCPMC5508866
OpenAlexW2577157584

What Socratic holds

Textmetadata
LicenceTDM
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.