Evidence map›Paper›PMID 25399696›Full record

ArticleOncogene2015

Regulation of cell cycle of hepatocellular carcinoma by NF90 through modulation of cyclin E1 mRNA stability.

W Jiang, H Huang, L Ding, P Zhu, H Saiyin, G Ji, J Zuo, D Han, Y Pan, D Ding and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.3field-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

51 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. LINC02167 stabilizes KSR1 mRNA in an mJournal of experimental & clinical cancer research : CR · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The Polyvalent Role of NF90 in RNA Biology.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
  11. Review
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  15. 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

18 authors at 4 institutions in 2 countries.

W JiangState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
H HuangState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
L DingState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
P ZhuState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
H SaiyinState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
G JiState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
J ZuoState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
D HanState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
Y PanDepartment of Biochemistry and Molecular Biology, Department of Urology, Mayo Clinic Cancer Center, Mayo Clinic College of Medicine, Rochester, NY, USA.
D DingState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
X MaState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
Y ZhangState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
J WuState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
Q YiDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
J O LiuDepartment of Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
H HuangState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
Y DangState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
L YuState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Fudan University, Shanghai, China.
Fudan University · CNCleveland Clinic Lerner College of Medicine · USJohns Hopkins Medicine · USMayo Clinic · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI Felicity Enders · 1985 to 2026
$151.3M
NCI NIH HHS P30 CA006973NCI NIH HHS P30 CA015083
6 · The paper itself

Abstract

Activation of cyclin E1, a key regulator of the G1/S cell-cycle transition, has been implicated in many cancers including hepatocellular carcinoma (HCC). Although much is known about the regulation of cyclin E1 expression and stability, its post-transcriptional regulation mechanism remains incompletely understood. Here, we report that nuclear factor 90 (NF90), a double-stranded RNA (dsRNA) binding protein, regulates cyclin E1 in HCC. We demonstrate that NF90 is upregulated in HCC specimens and that suppression of NF90 decreases HCC cell growth and delays G1/S transition. We identified cyclin E1 as a new target of NF90 and found a significant correlation between NF90 and cyclin E1 expression in HCC. The mRNA and protein levels of cyclin E1 were downregulated upon NF90 knockdown. Suppression of NF90 caused a decrease in the half-life of cyclin E1 mRNA, which was rescued by ectopic expression of NF90. Furthermore, NF90 bound to the 3' untranslated regions (3'UTRs) of cyclin E1 mRNA in vitro and in vivo. Knockdown of NF90 also inhibited tumor growth of HCC cell lines in mouse xenograft model. Moreover, we showed that inhibition of NF90 sensitized HCC cells to the cyclin-dependent kinase 2 (CDK2) inhibitor, roscovitine. Taken together, downregulation of NF90 in HCC cell lines can delay cell-cycle progression, inhibit cell proliferation, and reduce tumorigenic capacity in vivo. These results suggest that NF90 has an important role in HCC pathogenesis and that it can serve as a novel therapeutic target for HCC.

Indexed as

Cell CycleRNA Stability3' Untranslated RegionsAnimalsCarcinoma, HepatocellularCyclin-Dependent Kinase 2Cyclin EHumansLiver NeoplasmsMiceMice, Inbred BALB CNuclear Factor 90 ProteinsOncogene ProteinsPurinesRoscovitine3' Untranslated RegionsCCNE1 protein, humanCyclin-Dependent Kinase 2Cyclin EILF3 protein, humanNuclear Factor 90 ProteinsOncogene ProteinsPurinesRoscovitine

Identifiers

PMID25399696
PMCPMC4433881
OpenAlexW2020795077

What OpenQuestion holds

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LicenceTDM
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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.