Evidence map›Paper›PMID 27698442›Full record

ArticleScientific reports2016

Up-regulation of miR-95-3p in hepatocellular carcinoma promotes tumorigenesis by targeting p21 expression.

Jian Ye, Yufeng Yao, Qixue Song, Sisi Li, Zhenkun Hu, Yubing Yu, Changqing Hu, Xingwen Da, Hui Li, Qiuyun Chen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 43 citations in OpenAlex.

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  17. A brief overview of antitumoral actions of bruceine D.Exploration of targeted anti-tumor therapy · 2020
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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

11 authors at 2 institutions in 2 countries.

Jian YeKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, P. R. China.
Yufeng YaoKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, P. R. China.
Qixue SongKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, P. R. China.
Sisi LiKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, P. R. China.
Zhenkun HuKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, P. R. China.
Yubing YuKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, P. R. China.
Changqing HuKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, P. R. China.
Xingwen DaKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, P. R. China.
Hui LiKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, P. R. China.
Qiuyun ChenCenter for Cardiovascular Genetics, Department of Molecular Cardiology, Cleveland Clinic; Department of Molecular Medicine/CCLCM, Department of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, OH 44195, USA.
Qing K WangKey Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology and Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan, P. R. China.
Huazhong University of Science and Technology · CNCleveland Clinic · US

Funding

NGS in Large CAD Families: In-Depth Identification of Rare Risk Genomic VariantsR01HL121358 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI WANG, QING KENNETH · 2014 to 2017
$2.8M
Targeting Nav1.5 trafficking as a therapy for lethal genetic cardiac arrhythmiasR01HL126729 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI WANG, QING KENNETH · 2015 to 2018
$1.6M
NHLBI NIH HHS R01 HL121358NHLBI NIH HHS R01 HL126729
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most common malignant cancers. To elucidate new regulatory mechanisms for heptocarcinogenesis, we investigated the regulation of p21, a cyclin-dependent kinase (CDK) inhibitor encoded by CDKN1A, in HCC. The expression level of p21 is decreased with the progression of HCC. Luciferase assays with a luciferase-p21-3' UTR reporter and its serial deletions identified a 15-bp repressor element at the 3'-UTR of CDKN1A, which contains a binding site for miR-95-3p. Mutation of the binding site eliminated the regulatory effect of miR-95-3p on p21 expression. Posttranscriptional regulation of p21 expression by miR-95-3p is mainly on the protein level (suppression of translation). Overexpression of miR-95-3p in two different HCC cell lines, HepG2 and SMMC7721, significantly promoted cell proliferation, cell cycle progression and cell migration, whereas a miR-95-3p specific inhibitor decreased cell proliferation, cell cycle progression and cell migration. The effects of miR-95-3p on cellular functions were rescued by overexpression of p21. Overexpression of miR-95-3p promoted cell proliferation and tumor growth in HCC xenograft mouse models. Expression of miR-95-3p was significantly higher in HCC samples than in adjacent non-cancerous samples. These results demonstrate that miR-95-3p is a potential new marker for HCC and regulates hepatocarcinogenesis by directly targeting CDKN1A/p21 expression.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCarcinoma, HepatocellularCell CycleCell MovementCyclin-Dependent Kinase Inhibitor p21Hep G2 CellsHeterograftsHumansLiver NeoplasmsMaleMiceMicroRNAsNeoplasm TransplantationRNA, NeoplasmCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21MicroRNAsMIRN95 microRNA, humanRNA, Neoplasm

Identifiers

PMID27698442
PMCPMC5048429
OpenAlexW2529132047

What OpenQuestion holds

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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.