Evidence map›Paper›PMID 32332880›Full record

ArticleCell death & disease2020

E2F1 mediated DDX11 transcriptional activation promotes hepatocellular carcinoma progression through PI3K/AKT/mTOR pathway.

Yan Yu, Dan Zhao, Kongfei Li, Yubo Cai, Penglin Xu, Rui Li, Juan Li, Xiaolong Chen, Ping Chen, Guangying Cui

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 76 citations in OpenAlex.

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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

10 authors at 5 institutions in 2 countries.

Yan Yu *Precision Medicine Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Dan Zhao *Department of Oncology, The Third People's Hospital of Zhengzhou, Zhengzhou, 450000, China.
Kongfei Li *Department of Hematology, Yinzhou People's Hospital affiliated to Medical College of Ningbo University, Ningbo, 315000, China.
Yubo CaiZhejiang University School of Medicine, Hangzhou, 310058, China.
Penglin XuPrecision Medicine Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Rui LiNursing Department, The Third People's Hospital of Zhengzhou, Zhengzhou, 450000, China.
Juan LiKey Laboratory of Clinical Medicine, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Xiaolong ChenKey Laboratory of Clinical Medicine, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Ping ChenDepartment of Infectious Diseases, Shulan Hospital, Hangzhou, 310012, China. pingchendoctor@zju.edu.cn.
Guangying CuiPrecision Medicine Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. fcccuigy@zzu.edu.cn.ORCID http://orcid.org/0000-0003-3656-8100
First Affiliated Hospital of Zhengzhou University · CNZhengzhou People's Hospital · CNInfectious Diseases Society of America · USNingbo University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The DEAD/DEAH box helicase 11 (DDX11) plays vital roles in regulating the initiation of DNA replication. However, its precise function and regulation in hepatocellular carcinoma (HCC) have never been reported yet. In the current study, we found that DDX11 was overexpressed in HCC tissues. High DDX11 expression was positively correlated with large tumor size, tumor multiplicity, late tumor-node-metastasis (TNM) stage and poor prognosis. Additional, gain-of-function and loss-of-function experimental results revealed that DDX11 overexpression promoted HCC cell proliferation, migration, invasion and inhibited cell apoptosis in vitro. Overexpression of DDX11 also enhanced HCC tumorigenicity in vivo. Furthermore, DDX11 was transcriptionally regulated by transcription factor E2F1 in HCC, as demonstrated by chromatin immunoprecipitation (Ch-IP) and luciferase reporter assays. Mechanistically, E2F1/DDX11 axis promoted HCC cell proliferation, migration and invasion, at least in part, through activating PI3K/AKT/mTOR signaling pathway. Conclusively, our study demonstrates that E2F1-enhanced DDX11 expression promotes HCC progression through PI3K/AKT/mTOR pathway and DDX11 might be a potential therapeutic and prognostic target for HCC treatment.

Indexed as

Carcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationDEAD-box RNA HelicasesDisease ProgressionDNA HelicasesE2F1 Transcription FactorFemaleHumansLiver NeoplasmsMaleMiddle AgedPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionDDX11 protein, humanDEAD-box RNA HelicasesDNA HelicasesE2F1 protein, humanE2F1 Transcription FactorPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID32332880
PMCPMC7181644
OpenAlexW3019441095

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.