Evidence map›Paper›PMID 26771237›Full record

ArticleOncotarget2016

ZYG11A serves as an oncogene in non-small cell lung cancer and influences CCNE1 expression.

Xin Wang, Qi Sun, Chen Chen, Rong Yin, Xing Huang, Xuan Wang, Run Shi, Lin Xu, Binhui Ren

Open access · diamondAbstract 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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 28 citations in OpenAlex.

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  15. TFAP2A Induced KRT16 as an Oncogene in Lung Adenocarcinoma via EMT.International journal of biological sciences · 2019
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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

9 authors at 4 institutions in 1 country.

Xin WangDepartment of Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Cancer Institute of Jiangsu Province, Nanjing, Jiangsu, China.
Qi SunDepartment of Cardiothoracic Surgery at Jinling Hospital, Southern Medical University, Nanjing, Jiangsu, China.
Chen ChenDepartment of The Second Clinical College, Nanjing Medical University, Nanjing, Jiangsu, China.
Rong YinDepartment of Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Cancer Institute of Jiangsu Province, Nanjing, Jiangsu, China.
Xing HuangDepartment of Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Cancer Institute of Jiangsu Province, Nanjing, Jiangsu, China.
Xuan WangDepartment of The Fourth Clinical College, Nanjing Medical University, Nanjing, Jiangsu, China.
Run ShiDepartment of Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Cancer Institute of Jiangsu Province, Nanjing, Jiangsu, China.
Lin XuDepartment of Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Cancer Institute of Jiangsu Province, Nanjing, Jiangsu, China.
Binhui RenDepartment of Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Cancer Institute of Jiangsu Province, Nanjing, Jiangsu, China.
Jiangsu Cancer Hospital · CNNanjing Medical University · CNNanjing General Hospital of Nanjing Military Command · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

By analyzing The Cancer Genome Atlas (TCGA) database, we identified ZYG11A as a potential oncogene. We determined the expression of ZYG11A in NSCLC tissues and explored its clinical significance. And also evaluated the effects of ZYG11A on NSCLC cell proliferation, migration, and invasion both in vitro and in vivo. Our results show that ZYG11A is hyper-expressed in NSCLC tissues compared to adjacent normal tissues, and increased expression of ZYG11A is associated with a poor prognosis (HR: 2.489, 95%CI: 1.248-4.963, p = 0.010). ZYG11A knockdown induces cell cycle arrest and inhibits proliferation, migration, and invasion of NSCLC cells. ZYG11A knockdown also results in decreased expression of CCNE1. Over-expression of CCNE1 in cells with ZYG11A knockdown restores their oncogenic activities. Our data suggest that ZYG11A may serve as a novel oncogene promoting tumorigenicity of NSCLC cells by inducing cell cycle alterations and increasing CCNE1 expression.

Indexed as

AdenocarcinomaApoptosisBiomarkers, TumorBlotting, WesternCarcinoma, Non-Small-Cell LungCarcinoma, Squamous CellCell CycleCell Cycle ProteinsCell MovementCell ProliferationCyclin EFemaleFlow CytometryFollow-Up StudiesGene Expression Regulation, NeoplasticHumansBiomarkers, TumorCCNE1 protein, humanCell Cycle ProteinsCyclin EOncogene ProteinsRNA, MessengerZYG11A protein, humanbioinformaticsCCNE1NSCLConcogeneZYG11A

Identifiers

PMID26771237
PMCPMC4884973
OpenAlexW2275935873

What Socratic 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 Socratic graph.