Evidence map›Paper›PMID 27637078›Full record

ArticleOncotarget2016

miR-125b regulates differentiation and metabolic reprogramming of T cell acute lymphoblastic leukemia by directly targeting A20.

Zixing Liu, Kelly R Smith, Hung T Khong, Jingshan Huang, Eun-Young Erin Ahn, Ming Zhou, Ming Tan

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

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. MiRNAs in Hematopoiesis and Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2023
    Review
  5. Review
  6. miRNAs in Lymphocytic Leukaemias-The miRror of Drug Resistance.International journal of molecular sciences · 2022
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. The Emerging Roles of miR-125b in Cancers.Cancer management and research · 2020
    Review
  14. Review
  15. Article
  16. 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

7 authors at 4 institutions in 2 countries.

Zixing LiuMitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
Kelly R SmithMitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
Hung T KhongHuntsman Cancer Institute, University of Utah, Salt Lake City, Utah, USA.
Jingshan HuangSchool of Computing, University of South Alabama, Mobile, AL, USA.
Eun-Young Erin AhnMitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
Ming ZhouCancer Research Institute, Central South University, Changsha, Hunan, China.
Ming TanMitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
USA Mitchell Cancer Institute · USUniversity of South Alabama · USCentral South University · CNHuntsman Cancer Institute · US

Funding

SON-mediated gene expression and leukemiaR01CA190688 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI AHN, ERIN EUN-YOUNG · 2016 to 2021
$1.7M
Glucose metabolism and ErbB2-mediated cancer progressionR01CA149646 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI TAN, MING · 2011 to 2016
$1.4M
OmniSearch: A semantic search tool for discovering microRNAs' critical roles in hU01CA180982 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI HUANG, JINGSHAN · 2014 to 2016
$913k
NCI NIH HHS R01 CA149646NCI NIH HHS R01 CA190688NCI NIH HHS U01 CA180982
6 · The paper itself

Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematopoietic malignancy. Although it has been reported that overexpression of miR-125b leads to T-ALL development, the underlying mechanisms of miR-125b action are still unclear. The goal of this study is to delineate the role of miR-125b in T-ALL development. We found that miR-125b is highly expressed in undifferentiated leukemic T cells (CD4-negative) while its expression is low in differentiated T cells (CD4-positive). Overexpression of miR-125b increased the CD4-negative population in T cells, whereas depletion of miR-125b by miR-125b-sponge decreased the CD4-negative cell population. We identified that A20 (TNFAIP3) is a direct target of miR-125b in T cells. Overexpression of miR-125b also increased glucose uptake and oxygen consumption in T cells through targeting A20. Furthermore, restoration of A20 in miR-125b-overexpressing cells decreased the CD4-negative population in T cell leukemia, and decreased glucose uptake and oxygen consumption to the basal level of T cells transfected with vector. In conclusion, our data demonstrate that miR-125b regulates differentiation and reprogramming of T cell glucose metabolism via targeting A20. Since both de-differentiation and dysregulated glucose metabolism contribute to the development of T-cell leukemia, these findings provide novel insights into the understanding and treatment of T-ALL.

Indexed as

Cell DifferentiationCellular ReprogrammingEnergy MetabolismCD4-Positive T-LymphocytesGene Expression Regulation, LeukemicGlucoseHumansJurkat CellsMicroRNAsOxygen ConsumptionPrecursor T-Cell Lymphoblastic Leukemia-LymphomaSignal TransductionTransfectionTumor Necrosis Factor alpha-Induced Protein 3GlucoseMicroRNAsMIRN125 microRNA, humanTNFAIP3 protein, humanTumor Necrosis Factor alpha-Induced Protein 3A20differentiationlymphocytic leukemiamiR-125bT cell

Identifiers

PMID27637078
PMCPMC5346668
OpenAlexW2519006630

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.