Evidence map›Paper›PMID 28409330›Full record

ArticleInternational journal of hematology2017

MicroRNA-192 regulates cell proliferation and cell cycle transition in acute myeloid leukemia via interaction with CCNT2.

Shun Ke, Rui-Chao Li, Jun Lu, Fan-Kai Meng, Yi-Kuan Feng, Ming-Hao Fang

Abstract read
PubMed Publisher
In one paragraph

Article in International journal of hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  16. Review
  17. miR-192 Is Overexpressed and Promotes Cell Proliferation in Prostate Cancer.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2019
    Article
  18. MicroRNAs in Autoimmunity and Hematological Malignancies.International journal of molecular sciences · 2018
    Review
  19. Review
  20. Low miR-192 expression predicts poor prognosis in pediatric acute myeloid leukemia.Cancer biomarkers : section A of Disease markers · 2018
    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

6 authors at 2 institutions in 1 country.

Shun KeDepartment of Emergency Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Rui-Chao LiDepartment of General Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Jun LuDepartment of Emergency Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Fan-Kai MengDepartment of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Yi-Kuan FengDepartment of Emergency Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Ming-Hao FangDepartment of Emergency Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. fangmh@tjh.tjmu.edu.cn.
Huazhong University of Science and Technology · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are a class of small non-coding RNAs approximately 18-22 nucleotides in length, which play an important role in malignant transformation. The roles of miR-192 as an oncogene or tumor suppressor in solid tumors have been previously reported. However, little is known about the role of miR-192 in human acute myeloid leukemia. The results of the present study indicate that miR-192 is significantly downregulated in specimens from acute myeloid leukemia patients. Functional assays demonstrated that overexpression of miR-192 in NB4 and HL-60 cells significantly inhibited cell proliferation compared with that in control cells, and induced G0/G1 cell cycle arrest, cell differentiation, and apoptosis in vitro. Dual-luciferase reporter gene assays showed that miR-192 significantly suppressed the activity of a reporter gene containing the wild type 3'-UTR of CCNT2, but it did not suppress the activity of a reporter gene containing mutated 3'-UTR of CCNT2. QRT-PCR and Western blot assays showed that miR-192 significantly downregulated the expression of CCNT2 in human leukemia cells. Exogenous expression of CCNT2 attenuated the cell cycle arrest induced by miR-192 in NB4 and HL-60 cells. Collectively, miR-192 inhibits cell proliferation and induces G0/G1 cell cycle arrest in AML by regulating the expression of CCNT2.

Indexed as

3' Untranslated RegionsApoptosisCell CycleCell Cycle CheckpointsCell ProliferationCell Transformation, NeoplasticCyclin TDown-RegulationGene ExpressionHL-60 CellsHumansLeukemia, Myeloid, AcuteMicroRNAs3' Untranslated RegionsCCNT2 protein, humanCyclin TMicroRNAsMIRN192 microRNA, humanAcute myeloid leukemiaCCNT2Cell cyclemiR-192

Identifiers

PMID28409330
OpenAlexW2606787857

What OpenQuestion holds

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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.