Evidence map›Paper›PMID 27899822›Full record

ArticleCell death & disease2016

miR-150 exerts antileukemia activity in vitro and in vivo through regulating genes in multiple pathways.

Zhi Hong Fang, Si Li Wang, Jin Tao Zhao, Zhi Juan Lin, Lin Yan Chen, Rui Su, Si Ting Xie, Bing Z Carter, Bing Xu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 55 citations in OpenAlex.

  1. MircoRNAs predict and modulate responses to chemotherapy in leukemic patients.Naunyn-Schmiedeberg's archives of pharmacology · 2025
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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

9 authors at 2 institutions in 2 countries.

Zhi Hong FangDepartment of Hematology, The First Affiliated Hospital of Xiamen University, Xiamen 361003, China.
Si Li WangDepartment of Hematology, The First Affiliated Hospital of Xiamen University, Xiamen 361003, China.
Jin Tao ZhaoDepartment of Hematology, The First Affiliated Hospital of Xiamen University, Xiamen 361003, China.
Zhi Juan LinDepartment of Hematology, The First Affiliated Hospital of Xiamen University, Xiamen 361003, China.
Lin Yan ChenDepartment of Hematology, The First Affiliated Hospital of Xiamen University, Xiamen 361003, China.
Rui SuDepartment of Hematology, The First Affiliated Hospital of Xiamen University, Xiamen 361003, China.
Si Ting XieDepartment of Hematology, The First Affiliated Hospital of Xiamen University, Xiamen 361003, China.
Bing Z CarterSection of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA.
Bing XuDepartment of Hematology, The First Affiliated Hospital of Xiamen University, Xiamen 361003, China.
First Affiliated Hospital of Xiamen University · CNThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs, a class of small noncoding RNAs, have been implicated to regulate gene expression in virtually all important biological processes. Although accumulating evidence demonstrates that miR-150, an important regulator in hematopoiesis, is deregulated in various types of hematopoietic malignancies, the precise mechanisms of miR-150 action are largely unknown. In this study, we found that miR-150 is downregulated in samples from patients with acute lymphoblastic leukemia, acute myeloid leukemia, and chronic myeloid leukemia, and normalized after patients achieved complete remission. Restoration of miR-150 markedly inhibited growth and induced apoptosis of leukemia cells, and reduced tumorigenicity in a xenograft leukemia murine model. Microarray analysis identified multiple novel targets of miR-150, which were validated by quantitative real-time PCR and luciferase reporter assay. Gene ontology and pathway analysis illustrated potential roles of these targets in small-molecule metabolism, transcriptional regulation, RNA metabolism, proteoglycan synthesis in cancer, mTOR signaling pathway, or Wnt signaling pathway. Interestingly, knockdown one of four miR-150 targets (EIF4B, FOXO4B, PRKCA, and TET3) showed an antileukemia activity similar to that of miR-150 restoration. Collectively, our study demonstrates that miR-150 functions as a tumor suppressor through multiple mechanisms in human leukemia and provides a rationale for utilizing miR-150 as a novel therapeutic agent for leukemia treatment.

Indexed as

Gene Expression Regulation, LeukemicAnimalsApoptosisBase SequenceCell Line, TumorCell ProliferationDown-RegulationFemaleGene Expression ProfilingGene Knockdown TechniquesHumansLeukemiaLeukemia, Myeloid, AcuteMiceMice, NudeMicroRNAsMicroRNAsMIR150, human

Identifiers

PMID27899822
PMCPMC5059860
OpenAlexW2522386126

What Socratic 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 Socratic graph.