Evidence map›Paper›PMID 32159851›Full record

ArticleInternational journal of cancer2020

Dual-specificity phosphatase 6 plays a critical role in the maintenance of a cancer stem-like cell phenotype in human endometrial cancer.

Masaya Kato, Ichiro Onoyama, Sachiko Yoshida, Lin Cui, Keiko Kawamura, Keisuke Kodama, Emiko Hori, Yumiko Matsumura, Hiroshi Yagi, Kazuo Asanoma and 4 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of cancer, 2020. 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
1.5field-weighted citation impact, top 15% 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, 25 citations in OpenAlex.

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  14. DUSP7 inhibits cervical cancer progression by inactivating the RAS pathway.Journal of cellular and molecular medicine · 2021
    Article
  15. Article
  16. Targeting Phosphatases and Kinases: How to Checkmate Cancer.Frontiers in cell and developmental biology · 2021
    Review
  17. Article
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

14 authors at 2 institutions in 1 country.

Masaya KatoDepartment of Obstetrics and Gynecology, School of Medical Sciences, Kyushu University, Fukuoka, Japan.ORCID 0000-0003-2692-2014
Ichiro OnoyamaDepartment of Obstetrics and Gynecology, School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Sachiko YoshidaDepartment of Obstetrics and Gynecology, School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Lin CuiDepartment of Obstetrics and Gynecology, School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Keiko KawamuraDepartment of Obstetrics and Gynecology, School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Keisuke KodamaDepartment of Obstetrics and Gynecology, School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Emiko HoriDepartment of Obstetrics and Gynecology, School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Yumiko MatsumuraDepartment of Obstetrics and Gynecology, School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Hiroshi YagiDepartment of Obstetrics and Gynecology, School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Kazuo AsanomaDepartment of Obstetrics and Gynecology, School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Hideaki YahataDepartment of Obstetrics and Gynecology, School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Atsuo ItakuraDepartment of Obstetrics and Gynecology, School of Medical Sciences, Juntendo University, Tokyo, Japan.
Satoru TakedaDepartment of Obstetrics and Gynecology, School of Medical Sciences, Juntendo University, Tokyo, Japan.
Kiyoko KatoDepartment of Obstetrics and Gynecology, School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Kyushu University · JPJuntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The prognosis of patients with high-grade or advanced-stage endometrial cancer remains poor. As cancer stem-like cells (CSCs) are thought to be associated with endometrial cancers, it is essential to investigate the molecular mechanisms that regulate endometrial CSCs. Dual-specificity phosphatase 6 (DUSP6) functions as a negative-feedback regulator of MAPK-ERK1/2 signaling, but its role in endometrial cancer remains unknown. We investigated whether DUSP6 is involved in cancer cell stemness using endometrial cancer cell lines and specimens from endometrial cancer patients. DUSP6 induced the expression of CSC-related genes including ALDH1, Nanog, SOX2 and Oct4A, increased the population of cells in the G0/G1 phase, and promoted sphere formation ability. DUSP6 knockdown resulted in reduced cell invasion and metastasis, whereas DUSP6 overexpression inhibited apoptosis under serum-free conditions. Moreover, DUSP6 decreased phosphorylated ERK1/2 and increased phosphorylated Akt levels, which potentially induces CSC features. In patients with endometrial cancers, DUSP6 expression was determined using immunohistochemistry, and based on the results, the patients were dichotomized into high- and low-DUSP6-expression groups. Progression-free survival and overall survival were significantly shorter in the high-DUSP6-expression group. These results suggest that DUSP6 has potential value as a biomarker of CSCs and as a target of therapies designed to eliminate CSCs in endometrial cancer.

Indexed as

Up-RegulationAnimalsBiomarkers, TumorCell Line, TumorDisease ProgressionDual Specificity Phosphatase 6Endometrial NeoplasmsFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLung NeoplasmsMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Neoplasm TransplantationBiomarkers, TumorDual Specificity Phosphatase 6DUSP6 protein, humanMAPK1 protein, humanMAPK3 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-aktAktcancer stem-like cellDUSP6endometrial cancerERK1/2

Identifiers

PMID32159851
PMCPMC7496376
OpenAlexW3011192643

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.