Evidence map›Paper›PMID 29150975›Full record

ArticleCancer science2018

Downregulation of dual-specificity phosphatase 4 enhances cell proliferation and invasiveness in colorectal carcinomas.

Michihiro Ichimanda, Naoki Hijiya, Yoshiyuki Tsukamoto, Tomohisa Uchida, Chisato Nakada, Tomonori Akagi, Tsuyoshi Etoh, Hidekatsu Iha, Masafumi Inomata, Mutsuhiro Takekawa and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

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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 2 institutions in 1 country.

Michihiro IchimandaDepartment of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan.
Naoki HijiyaDepartment of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan.ORCID http://orcid.org/0000-0003-3775-8395
Yoshiyuki TsukamotoDepartment of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan.
Tomohisa UchidaDepartment of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan.
Chisato NakadaDepartment of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan.
Tomonori AkagiDepartment of Gastroenterological and Pediatric Surgery, Faculty of Medicine, Oita University, Oita, Japan.
Tsuyoshi EtohDepartment of Gastroenterological and Pediatric Surgery, Faculty of Medicine, Oita University, Oita, Japan.
Hidekatsu IhaDepartment of Microbiology, Faculty of Medicine, Oita University, Oita, Japan.
Masafumi InomataDepartment of Gastroenterological and Pediatric Surgery, Faculty of Medicine, Oita University, Oita, Japan.
Mutsuhiro TakekawaDivision of Cell Signaling and Molecular Medicine, Institute of Medical Sciences, University of Tokyo, Tokyo, Japan.
Masatsugu MoriyamaDepartment of Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan.
Oita University · JPTokyo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is widely accepted that aberrant activation of the Wnt signaling pathway is responsible for the development of precursor lesions of colorectal cancer (CRC). However, the molecular mechanisms involved in the process of progression from these precursor lesions to invasive lesions of CRC are not fully understood. Recently, we reported that constitutive activation of MAPK accompanied by downregulation of dual-specificity phosphatase 4 (DUSP4), a MAPK phosphatase, contributes to the progression of precursor lesions in the pancreas. In this study, we found that downregulation of DUSP4 was related to constitutive activation of ERKs in CRC cells. Restoration of DUSP4 resulted in inactivation of ERKs, leading to suppression of both proliferation and invasiveness, as shown by treatment with an MEK inhibitor. Furthermore, immunohistochemistry revealed that DUSP4 expression was upregulated in the superficial region of CRC tissue, whereas it was significantly downregulated in the deep region. In contrast, ERKs in the deep region were markedly hyperactivated compared to those in the superficial region. These results suggest that activation of the MAPK signaling pathway caused by downregulation of DUSP4 is responsible for progression of CRCs and would be a promising therapeutic target.

Indexed as

Down-RegulationAgedCell Line, TumorCell ProliferationColorectal NeoplasmsDual-Specificity PhosphatasesExtracellular Signal-Regulated MAP KinasesFemaleGene Expression Regulation, NeoplasticHCT116 CellsHumansMaleMiddle AgedMitogen-Activated Protein Kinase PhosphatasesNeoplasm InvasivenessPhosphorylationDual-Specificity PhosphatasesDUSP4 protein, humanExtracellular Signal-Regulated MAP KinasesMitogen-Activated Protein Kinase Phosphatasescolorectal carcinomaDUSP4invasionMAPK signallingproliferation

Identifiers

PMID29150975
PMCPMC5765293
OpenAlexW2770281344

What OpenQuestion holds

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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.