Evidence map›Paper›PMID 26840256›Full record

ArticleOncotarget2016

Cullin 4A (CUL4A), a direct target of miR-9 and miR-137, promotes gastric cancer proliferation and invasion by regulating the Hippo signaling pathway.

Jun Deng, Wan Lei, Xiaojun Xiang, Ling Zhang, Jun Lei, Yu Gong, Meijiao Song, Yi Wang, Ziling Fang, Feng Yu and 5 more

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

39 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. International journal of molecular sciences · 2026
    Article
  3. The Regulation and Function of Hippo/YAP Pathway in Cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    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

15 authors.

Jun DengDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
Wan LeiDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
Xiaojun XiangDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
Ling ZhangDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
Jun LeiDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
Yu GongDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
Meijiao SongDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
Yi WangDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
Ziling FangDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
Feng YuDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
Miao FengDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
Ze SunDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
Jun ChenDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
Zhengyu ZhanDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.
Jianping XiongDepartment of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, PR China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although Cullin 4A (CUL4A) is mutated or amplified in several human cancer types, its role in gastric cancer (GC) and the mechanisms underlying its regulation remain largely uncharacterized. In the present study, we report that the expression of CUL4A significantly correlated with the clinical stage of the tumor and lymph node metastasis, and survival rates were lower in GC patients with higher levels of CUL4A than in patients with lower CUL4A levels. The upregulation of CUL4A promoted GC cell proliferation and epithelial-mesenchymal transition (EMT) by downregulating LATS1-Hippo-YAP signaling. Knocking down CUL4A had the opposite effect in vitro and in vivo. Interestingly, CUL4A expression was inhibited by the microRNAs (miRNAs), miR-9 and miR-137, which directly targeted the 3'-UTR of CUL4A. Overexpression of miR-9 and miR-137 downregulated the CUL4A-LATS1-Hippo signaling pathway and suppressed GC cell proliferation and invasion in vitro. Taken together, our findings demonstrate that perturbations to miR-9/137-CUL4A-Hippo signaling contribute to gastric tumorigenesis, and suggest potential therapeutic targets for the future treatment of GC.

Indexed as

3' Untranslated RegionsAdultAgedAnimalsCell Line, TumorCell MovementCell ProliferationCullin ProteinsFemaleGene Expression Regulation, NeoplasticHippo Signaling PathwayHumansLymphatic MetastasisMaleMice, Inbred BALB CMice, Nude3' Untranslated RegionsCUL4A protein, humanCullin ProteinsMicroRNAsMIRN137 microRNA, humanMIRN92 microRNA, humanProtein Serine-Threonine KinasesCUL4Agastric cancerHippomiR-137miR-9

Identifiers

PMID26840256
PMCPMC4891102

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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.