Evidence map›Paper›PMID 30015844›Full record

ArticleMolecular medicine reports2018

Downregulation of microRNA‑21 expression inhibits proliferation, and induces G1 arrest and apoptosis via the PTEN/AKT pathway in SKM‑1 cells.

Guang Li, Yanping Song, Gangcan Li, Jingjing Ren, Jia Xie, Yunjie Zhang, Fei Gao, Jiao Mu, Jinqian Dai

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  4. 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 1 country.

Guang LiInstitute of Hematopathy, Xi'an Central Hospital, Xi'an, Shaanxi 710003, P.R. China.
Yanping SongInstitute of Hematopathy, Xi'an Central Hospital, Xi'an, Shaanxi 710003, P.R. China.
Gangcan LiInstitute of Hematopathy, Xi'an Central Hospital, Xi'an, Shaanxi 710003, P.R. China.
Jingjing RenInstitute of Hematopathy, Xi'an Central Hospital, Xi'an, Shaanxi 710003, P.R. China.
Jia XieInstitute of Hematopathy, Xi'an Central Hospital, Xi'an, Shaanxi 710003, P.R. China.
Yunjie ZhangInstitute of Hematopathy, Xi'an Central Hospital, Xi'an, Shaanxi 710003, P.R. China.
Fei GaoInstitute of Hematopathy, Xi'an Central Hospital, Xi'an, Shaanxi 710003, P.R. China.
Jiao MuInstitute of Hematopathy, Xi'an Central Hospital, Xi'an, Shaanxi 710003, P.R. China.
Jinqian DaiInstitute of Hematopathy, Xi'an Central Hospital, Xi'an, Shaanxi 710003, P.R. China.
First Hospital of Xi'an · CNXian Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myelodysplastic syndromes (MDS) are characterized by ineffective hematopoiesis and may progress to acute myeloid leukemia (AML). MicroRNAs (miRNA/miRs) as oncogenes or tumor suppressors regulate a number of biological processes including cell proliferation, cell cycle and apoptosis in different types of cancer cells. Recently, it has been reported that miR‑21 as an oncogene is overexpressed and directly targets SMAD‑7 in MDS. However, little is known about the mechanism of miR‑21 in the progression of MDS. In the present study, the role of miR‑21 in the proliferation and apoptosis of SKM‑1 cells, an acute myeloid leukemia cell line established in the AML/MDS leukemic phase was investigated. The present results demonstrated that downregulation of miR‑21 inhibited proliferation, induced apoptosis and caused G1 phase cell cycle arrest of SKM‑1 cells. In addition, the expression levels of apoptosis regulator Bcl‑2 (bcl2), cyclinD1 and phosphorylated‑protein kinase B (AKT) were significantly decreased in SKM‑1 cells transfected with the miR‑21 inhibitor, whilst the expression levels of phosphatase and tensin homolog (PTEN), bcl‑associated protein X (bax) and cleaved caspase 3 were significantly elevated. Furthermore, knockdown of Akt by small interfering (si)RNA significantly increased the expression of bax, cleaved caspase 3 and reduced the expression of bcl2 and cyclinD1 in SKM‑1 cells. Taken together, these data indicate that miR‑21 targets the PTEN/AKT pathway in the pathogenesis of MDS and could be a potential target for MDS therapy.

Indexed as

ApoptosisCell ProliferationAntagomirsbcl-2-Associated X ProteinCaspase 3Cell Line, TumorCyclin D1Down-RegulationG1 Phase Cell Cycle CheckpointsHumansMicroRNAsMyelodysplastic SyndromesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2PTEN PhosphohydrolaseRNA InterferenceAntagomirsbcl-2-Associated X ProteinBCL2 protein, humanCaspase 3Cyclin D1MicroRNAsMIRN21 microRNA, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2PTEN PhosphohydrolasePTEN protein, humanRNA, Small Interfering

Identifiers

PMID30015844
PMCPMC6102657
OpenAlexW2844955198

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.