Evidence map›Paper›PMID 25149542›Full record

ArticleOncotarget2014

ATF3 functions as a novel tumor suppressor with prognostic significance in esophageal squamous cell carcinoma.

Jian-Jun Xie, Yang-Min Xie, Bo Chen, Feng Pan, Jin-Cheng Guo, Qing Zhao, Jin-Hui Shen, Zhi-Yong Wu, Jian-Yi Wu, Li-Yan Xu and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. 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
6.5field-weighted citation impact, top 3% 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, 70 citations in OpenAlex.

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  8. ATF3 in atherosclerosis: a controversial transcription factor.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  9. Journal of microbiology and biotechnology · 2022
    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

11 authors at 3 institutions in 1 country.

Jian-Jun XieKey Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Medical College of Shantou University, Shantou 515041, P. R. China. Department of Biochemistry and Molecular Biology, Medical College of Shantou University, Shantou 515041, P. R. China.
Yang-Min XieKey Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Medical College of Shantou University, Shantou 515041, P. R. China. Department of Experimental Animal Center, Medical College of Shantou University, Shantou 515041, P. R. China.
Bo ChenKey Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Medical College of Shantou University, Shantou 515041, P. R. China. Institute of Oncologic Pathology, Medical College of Shantou University, Shantou 515041, P. R. China.
Feng PanKey Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Medical College of Shantou University, Shantou 515041, P. R. China. Department of Biochemistry and Molecular Biology, Medical College of Shantou University, Shantou 515041, P. R. China.
Jin-Cheng GuoKey Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Medical College of Shantou University, Shantou 515041, P. R. China. Department of Biochemistry and Molecular Biology, Medical College of Shantou University, Shantou 515041, P. R. China.
Qing ZhaoKey Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Medical College of Shantou University, Shantou 515041, P. R. China. Institute of Oncologic Pathology, Medical College of Shantou University, Shantou 515041, P. R. China.
Jin-Hui ShenDepartment of Pathology, Shantou Central Hospital, Affiliated Shantou Hospital of Sun Yat-Sen University, Shantou 515041, P. R. China.
Zhi-Yong WuKey Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Medical College of Shantou University, Shantou 515041, P. R. China. Department of Oncologic Surgery, Shantou Central Hospital, Affiliated Shantou Hospital of Sun Yat-Sen University, Shantou 515041, P. R. China.
Jian-Yi WuKey Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Medical College of Shantou University, Shantou 515041, P. R. China. Department of Biochemistry and Molecular Biology, Medical College of Shantou University, Shantou 515041, P. R. China.
Li-Yan XuKey Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Medical College of Shantou University, Shantou 515041, P. R. China. Institute of Oncologic Pathology, Medical College of Shantou University, Shantou 515041, P. R. China.
En-Min LiKey Laboratory of Molecular Biology in High Cancer Incidence Coastal Chaoshan Area of Guangdong Higher Education Institutes, Medical College of Shantou University, Shantou 515041, P. R. China. Department of Biochemistry and Molecular Biology, Medical College of Shantou University, Shantou 515041, P. R. China.
Shantou University Medical College · CNShantou University · CNShantou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ATF3 was a transcription factor involved in the progression of certain cancers. Here, we sought to explore the expression and biological function of ATF3 in esophageal squamous cell carcinomas (ESCC). The prognostic significance of ATF3 expression was evaluated in 150 ESCC samples and 21 normal squamous cell epithelium tissues. Results showed that ATF3 was down-regulated in ESCC lesions compared with paired non-cancerous tissues and low tumorous ATF3 expression significantly correlated with shorter overall survival (OS) and disease-free survival (DFS). Cox regression analysis confirmed that ATF3 expression was an independent prognostic factor. Experimentally, forced expression of ATF3 led to decreased growth and invasion properties of ESCC cells in vitro and in vivo, whereas knockdown of ATF3 did the opposite. Furthermore, ATF3 upregulated the expression of MDM2 by increasing the nuclear translocation of P53 and formed an ATF3/MDM2/MMP-2 complex that facilitated MMP-2 degradation, which subsequently led to inhibition of cell invasion. Finally, we showed that Cisplatin could restrain the invasion of ESCC cells by inducing the expression of ATF3 via P53 signaling. Combined, our findings highlight a suppressed role for ATF3 in ESCC and targeting ATF3 might be a potential therapeutic strategy.

Indexed as

Activating Transcription Factor 3AnimalsAntineoplastic AgentsBiomarkers, TumorCarcinoma, Squamous CellCell Line, TumorCell MovementCell ProliferationCisplatinDisease-Free SurvivalDose-Response Relationship, DrugEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateActivating Transcription Factor 3Antineoplastic AgentsATF3 protein, humanBiomarkers, TumorCisplatinMatrix Metalloproteinase 2MDM2 protein, humanMMP2 protein, humanProto-Oncogene Proteins c-mdm2TP53 protein, humanTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID25149542
PMCPMC4226705
OpenAlexW1561655211

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.