Evidence map›Paper›PMID 24919811›Full record

ArticleInternational journal of molecular medicine2014

MicroRNA-206 overexpression promotes apoptosis, induces cell cycle arrest and inhibits the migration of human hepatocellular carcinoma HepG2 cells.

Weiwei Liu, Chuanming Xu, Huifang Wan, Chunju Liu, Can Wen, Hongfei Lu, Fusheng Wan

Open access · bronzeAbstract read
In one paragraph

Article in International journal of molecular medicine, 2014. 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
1.6field-weighted citation impact, top 19% 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, 49 citations in OpenAlex.

  1. Article
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  8. Differential expression of angiogenesis-related miRNAs andArchives of medical science : AMS · 2020
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  9. Review
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  15. The oncomir face of microRNA-206: A permanent miR-206 transfection study.Experimental biology and medicine (Maywood, N.J.) · 2018
    Article
  16. The Role ofThe oncologist · 2018
    Review
  17. Article
  18. Article
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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

7 authors at 2 institutions in 1 country.

Weiwei LiuDepartment of Biochemistry and Molecular Biology, Basic Medical College of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Chuanming XuDepartment of Biochemistry and Molecular Biology, Basic Medical College of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Huifang WanMedical Experiment Education Department of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Chunju LiuDepartment of Clinical Laboratory, The Affiliated Hospital of Jiangxi College of Chinese Medicine, Nanchang, Jiangxi 330006, P.R. China.
Can WenDepartment of Biochemistry and Molecular Biology, Basic Medical College of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Hongfei LuDepartment of Biochemistry and Molecular Biology, Basic Medical College of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Fusheng WanDepartment of Biochemistry and Molecular Biology, Basic Medical College of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Nanchang University · CNAffiliated Hospital of Jiangxi College of TCM · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA-206 (miR-206) is known to regulate cell proliferation and migration and is involved in various types of cancer. However, the role of miR-206 in human hepatocellular carcinoma (HHC) has not been previously reported. In the present study, the expression of Notch3 in HCC and adjacent non-neoplastic tissue was immunohistochemically assessed on formalin-fixed, paraffin-embedded sections. miR-206 mimics were transiently transfected into HepG2 cells using Lipofectamine™ 2000. Subsequently, we evaluated the role of miR-206 in cell proliferation, apoptosis, cell cycle arrest and migration by MTS assay, Hoechst 33342 staining, Annexin V-FITC/PI assay, flow cytometry and wound healing assay. Using quantitative reverse transcription polymerase chain reaction (qRT‑PCR) and western blot analysis, we detected the expression of Notch3, Bax, Bcl-2, Hes1, p57 and matrix metalloproteinase (MMP)-9 at the mRNA and protein level, respectively. In addition, we measured the expression of miR-206 at the mRNA level and that of caspase-3 at the protein level. After miR-206 was upregulated in HepG2 cells, Notch3, Hes1, Bcl-2 and MMP-9 were downregulated both at the mRNA and protein level, whereas p57 and Bax were upregulated. Cleaved caspase-3 protein expression was also markedly increased. Cell proliferation was significantly attenuated and apoptosis was markedly increased. Furthermore, miR-206 overexpression induced cell cycle arrest and inhibited the migration of HepG2 cells. Taken together, our results uggest that miR-206 is a potential regulator of apoptosis, the cell cycle and migration in HepG2 cells and that it has the potential for use in the targeted therapy of HCC and is a novel tumor suppressor.

Indexed as

ApoptosisCarcinoma, HepatocellularCell Cycle CheckpointsCell MovementGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHep G2 CellsHumansLiver NeoplasmsMicroRNAsNeoplasm ProteinsMicroRNAsMIRN206 microRNA, humanNeoplasm Proteins

Identifiers

PMID24919811
PMCPMC4094593
OpenAlexW2030520840

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LicenceCC BY
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Registered trials

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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.