Evidence map›Paper›PMID 30987656›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

A positive feedback loop consisting of C12orf59/NF-κB/CDH11 promotes gastric cancer invasion and metastasis.

Jia-Xing Zhang, Wei-Ling He, Zi-Hao Feng, Dong-Liang Chen, Ying Gao, Ying He, Kai Qin, Zhou-San Zheng, Cui Chen, Hui-Wen Weng and 4 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 1 institution in 1 country.

Jia-Xing Zhang *The State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, No. 651, Dongfeng Road East, 510060, Guangzhou, Guangdong Province, People's Republic of China.
Wei-Ling He *Department of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Zi-Hao Feng *Department of Urology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Dong-Liang Chen *The State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, No. 651, Dongfeng Road East, 510060, Guangzhou, Guangdong Province, People's Republic of China.
Ying GaoDepartment of Oncology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Ying HeDepartment of Oncology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Kai QinDepartment of Extracorporeal Circulation, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Zhou-San ZhengDepartment of Oncology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Cui ChenDepartment of Oncology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Hui-Wen WengDepartment of Oncology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Miao YunThe State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, No. 651, Dongfeng Road East, 510060, Guangzhou, Guangdong Province, People's Republic of China.
Sheng YeDepartment of Oncology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510080, Guangdong Province, People's Republic of China.
Rui-Hua XuThe State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, No. 651, Dongfeng Road East, 510060, Guangzhou, Guangdong Province, People's Republic of China. xurh@sysucc.org.cn.
Dan XieThe State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, No. 651, Dongfeng Road East, 510060, Guangzhou, Guangdong Province, People's Republic of China. xiedan@sysucc.org.cn.
Sun Yat-sen University · CN

Funding

National Key R&D Program of China 2016YFC1302305National Key R&D Program of China 2017YFC1309001National Natural Science Foundation of China 81572359National Natural Science Foundation of China 81772513National Natural Science Foundation of China 81772514Pearl River S&T Nova Program of Guangzhou 201806010005
6 · The paper itself

Abstract

backgroundMetastasis remains the main cause of cancer-related death for gastric cancer (GC) patients, but the mechanisms are poorly understood. Using The Cancer Genome Atlas (TCGA) data base and bioinformatics analyses, we identified C12orf59 might act as a potential oncogenic protein in GC.

methodsWe investigate the expression pattern and clinical significance of C12orf59 in two independent cohorts of GC samples. In the training cohort, we used the X-tile program software to generate the optimal cutoff value for C12orf59 expression in order to classify patients accurately according to clinical outcome. In the validation cohort, this derived cutoff score was applied to exam the association of C12orf59 expression with survival outcome. A series of in vivo and in vitro assays were then performed to investigate the function of C12orf59 in GC.

resultsC12orf59 was significantly upregulated, and associated with poor survival outcome in two cohorts of GC samples. Gain- and loss of- function studies demonstrated C12orf59 promotes GC cell invasive and metastatic capacity both in vitro and in vivo, and induces epithelial-mesenchymal transition and angiogenesis. Mechanically, C12orf59 exerts oncogenic functions by up-regulating CDH11 expression via NF-κB signaling. Interesting, CDH11 could in turn promote NF-κB bind to C12orf59's promoter and form a positive feedback loop to sustain the metastatic ability of GC cells. Additionally, downregulation of miR-654-5p is another important mechanism for C12orf59 overexpression in GC.

conclusionOur finding suggested the newly identified C12orf59/NF-κB/CDH11 feedback loop may represent a new strategy for GC treatment.

Indexed as

Gene Expression Regulation, NeoplasticSignal TransductionAdultAgedBiomarkers, TumorCadherinsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFemaleHumansMaleMicroRNAsMiddle AgedNeoplasm InvasivenessNeoplasm MetastasisBiomarkers, TumorCadherinsMicroRNAsMIRN654 microRNA, humanNF-kappa BOncogene Proteinsosteoblast cadherinC12orf59CDH11Gastric cancerMetastasisNF-κB

Identifiers

PMID30987656
PMCPMC6463669
OpenAlexW2938604645

What OpenQuestion holds

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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.