Evidence map›Paper›PMID 26881775›Full record

ArticlePloS one2016

CD10-Equipped Melanoma Cells Acquire Highly Potent Tumorigenic Activity: A Plausible Explanation of Their Significance for a Poor Prognosis.

Junna Oba, Takeshi Nakahara, Akiko Hashimoto-Hachiya, Min Liu, Takeru Abe, Akihito Hagihara, Takehiko Yokomizo, Masutaka Furue

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

8 citing papers in PubMed, 12 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

8 authors at 2 institutions in 1 country.

Junna ObaDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Takeshi NakaharaDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Akiko Hashimoto-HachiyaDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Min LiuDepartment of Biochemistry, Juntendo University School of Medicine, Tokyo, Japan.
Takeru AbeDepartment of Health Services Management and Policy, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Akihito HagiharaDepartment of Health Services Management and Policy, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Takehiko YokomizoDepartment of Biochemistry, Juntendo University School of Medicine, Tokyo, Japan.
Masutaka FurueDepartment of Dermatology, Graduate 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

CD10 has been widely used in cancer diagnosis. We previously demonstrated that its expression in melanoma increased with tumor progression and predicted poor patient survival. However, the mechanism by which CD10 promotes melanoma progression remains unclear. In order to elucidate the role of CD10 in melanoma, we established CD10-overexpressing A375 melanoma cells and performed DNA microarray and qRT-PCR analyses to identify changes in the gene expression profile. The microarray analysis revealed that up-regulated genes in CD10-A375 were mostly involved in cell proliferation, angiogenesis, and resistance to apoptosis; down-regulated genes mostly belonged to the categories associated with cell adhesion and migration. Accordingly, in functional experiments, CD10-A375 showed significantly greater cell proliferation in vitro and higher tumorigenicity in vivo; CD10 enzymatic inhibitors, thiorphan and phosphoramidon, significantly blocked the tumor growth of CD10-A375 in mice. In migration and invasion assays, CD10-A375 displayed lower migratory and invasive capacity than mock-A375. CD10 augmented melanoma cell resistance to apoptosis mediated by etoposide and gemcitabine. These findings indicate that CD10 may promote tumor progression by regulating the expression profiles of genes related to cell proliferation, angiogenesis, and resistance to apoptosis.

Indexed as

AnimalsAntineoplastic AgentsCarcinogenesisCell Line, TumorCell MovementCell ProliferationDrug Resistance, NeoplasmGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMelanomaMice, Inbred BALB CNeoplasm InvasivenessNeprilysinPrognosisTransfectionAntineoplastic AgentsNeprilysin

Identifiers

PMID26881775
PMCPMC4755541
OpenAlexW2277193863

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.