Evidence map›Paper›PMID 33201900›Full record

ArticlePloS one2020

MiR-424-5p regulates cell cycle and inhibits proliferation of hepatocellular carcinoma cells by targeting E2F7.

Yichao Zhao, Chaoqian Zhu, Qing Chang, Peng Peng, Jie Yang, Chunmei Liu, Yang Liu, Xiaonan Chen, Yuanguang Liu, Ran Cheng and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-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

29 citing papers in PubMed, 37 citations in OpenAlex.

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  12. Role of miR-424 in the carcinogenesis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Review
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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

14 authors at 1 institution in 1 country.

Yichao ZhaoDepartment of Hepatobiliary Surgery, Tangshan Gongren Hospital, Tangshan, China.
Chaoqian ZhuDepartment of Hepatobiliary Surgery, Tangshan Gongren Hospital, Tangshan, China.
Qing ChangDepartment of Head and Neck Surgery, Tangshan Gongren Hospital, Tangshan, China.
Peng PengDepartment of Hepatobiliary Surgery, Tangshan Gongren Hospital, Tangshan, China.
Jie YangDepartment of Geriatrics, Tangshan Gongren Hospital, Tangshan, China.
Chunmei LiuDepartment of Hepatobiliary Surgery, Tangshan Gongren Hospital, Tangshan, China.
Yang LiuDepartment of Hepatobiliary Surgery, Tangshan Gongren Hospital, Tangshan, China.
Xiaonan ChenDepartment of Hepatobiliary Surgery, Tangshan Gongren Hospital, Tangshan, China.
Yuanguang LiuDepartment of Hepatobiliary Surgery, Tangshan Gongren Hospital, Tangshan, China.
Ran ChengDepartment of Hepatobiliary Surgery, Tangshan Gongren Hospital, Tangshan, China.
Yijie WuDepartment of Hepatobiliary Surgery, Tangshan Gongren Hospital, Tangshan, China.
Xiaotang WuShanghai Engineering Research Center of Pharmaceutical Translation, Shanghai, China.
Liang HuShanghai Engineering Research Center of Pharmaceutical Translation, Shanghai, China.
Jun YinDepartment of Hepatobiliary Surgery, Tangshan Gongren Hospital, Tangshan, China.ORCID 0000-0002-6297-4121
Tangshan Gongren Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study aims to explore the mechanism of the miR-424-5p/E2F7 axis in hepatocellular carcinoma (HCC) and provide new ideas for targeted therapy of HCC.

methodsBioinformatics analysis was used to identify the target differentially expressed miRNA in HCC and predict its target gene. qRT-PCR was employed to verify the expression of miR-424-5p and E2F7 mRNA in HCC cells. Western blot was performed to detect the effect of miR-424-5p ectopic expression on the protein expression of E2F7. CCK-8 was used to detect proliferative activity of HCC cells and flow cytometry was carried out for analyzing cell cycle distribution. Dual luciferase reporter assay was conducted to verify the direct targeting relationship between miR-424-5p and E2F7.

resultsWe observed that miR-424-5p was down-regulated in HCC cells. CCK-8 showed that overexpression of miR-424-5p inhibited cell proliferation, and flow cytometry showed that miR-424-5p could block cells in G0/G1 phase. E2F7 was up-regulated in HCC cells, and E2F7 overexpression could facilitate the proliferative ability of HCC cells and promote the cell cycle progressing from G0/G1 to S phase. Furthermore, dual-luciferase reporter assay indicated that miR-424-5p could directly down-regulate E2F7 expression. Analysis on cell function demonstrated that miR-424-5p inhibited the proliferation of HCC cells and blocked cell cycle at G0/G1 phase by targeting E2F7.

conclusionOur results proved that E2F7 was a direct target of miR-424-5p, and miR-424-5p could regulate cell cycle and further inhibit the proliferation of HCC cells by targeting E2F7.

Indexed as

Carcinoma, HepatocellularCell CycleCell Line, TumorCell ProliferationDown-RegulationE2F7 Transcription FactorGene Expression Regulation, NeoplasticHEK293 CellsHumansLiver NeoplasmsMicroRNAsE2F7 protein, humanE2F7 Transcription FactorMicroRNAsMIRN424 microrna, human

Identifiers

PMID33201900
PMCPMC7671513
OpenAlexW3101787818

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.