Evidence map›Paper›PMID 29966001›Full record

ArticlePloS one2018

The stress response gene ATF3 is a direct target of the Wnt/β-catenin pathway and inhibits the invasion and migration of HCT116 human colorectal cancer cells.

Makoto Inoue, Yohei Uchida, Makoto Edagawa, Manabu Hirata, Jun Mitamura, Daiki Miyamoto, Kenji Taketani, Shigeki Sekine, Junya Kawauchi, Shigetaka Kitajima

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.3field-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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  19. ATF-3 expression inhibits melanoma growth by downregulating ERK and AKT pathways.Laboratory investigation; a journal of technical methods and pathology · 2021
    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

10 authors at 1 institution in 1 country.

Makoto InoueDepartment of Biochemical Genetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Yohei UchidaDepartment of Biochemical Genetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Makoto EdagawaDepartment of Biochemical Genetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Manabu HirataDepartment of Biochemical Genetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Jun MitamuraDepartment of Biochemical Genetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Daiki MiyamotoDepartment of Biochemical Genetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Kenji TaketaniDepartment of Biochemical Genetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Shigeki SekinePathology Division, National Cancer Center Research Institute, Tokyo, Japan.
Junya KawauchiDepartment of Biochemical Genetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.
Shigetaka KitajimaDepartment of Biochemical Genetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan.ORCID 0000-0003-3959-6107
Tokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant Wnt/β-catenin signaling is implicated in tumorigenesis and the progression of human colorectal cancers, and mutations in the components of the Wnt/β-catenin signaling pathway are observed in the majority of patients. Therefore, extensive studies on the Wnt signaling pathway and its target genes are crucial to understand the molecular events of tumorigenesis and develop an efficacious therapy. In this study, we showed that the stress response gene ATF3 is transcriptionally activated by the binding of β-catenin and TCF4 to the redundant TCF4 site at the proximal promoter region of the ATF3 gene, indicating that ATF3 is a direct target of the Wnt/β-catenin pathway. The loss of function or overexpression studies showed that ATF3 inhibited the migration or invasion of HCT116 cells. The expression of some MMP and TIMP genes and the ratio of MMP2/9 to TIMP3/4 mRNAs was differentially regulated by ATF3. Therefore, though ATF3 is activated downstream of the Wnt/β-catenin pathway, it acts as a negative regulator of the migration and invasion of HCT116 human colon cancer cells exhibiting aberrant Wnt/β-catenin activity. ATF3 is a candidate biomarker and target for human colorectal cancer treatment and prevention.

Indexed as

Activating Transcription Factor 3beta CateninBiomarkers, TumorCarcinogenesisCell MovementCell ProliferationColorectal NeoplasmsGene Expression Regulation, NeoplasticHCT116 CellsHumansMatrix Metalloproteinase 2Matrix Metalloproteinase 9Neoplasm InvasivenessProtein BindingTissue Inhibitor of Metalloproteinase-3Transcription Factor 4Activating Transcription Factor 3ATF3 protein, humanbeta CateninBiomarkers, TumorCTNNB1 protein, humanMatrix Metalloproteinase 2Matrix Metalloproteinase 9MMP2 protein, humanMMP9 protein, humanTCF4 protein, humanTIMP3 protein, humanTissue Inhibitor of Metalloproteinase-3Transcription Factor 4

Identifiers

PMID29966001
PMCPMC6028230
OpenAlexW2810456907

What OpenQuestion 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 OpenQuestion graph.