Evidence map›Paper›PMID 31578411›Full record

ArticleScientific reports2019

Acquisition of a side population fraction augments malignant phenotype in ovarian cancer.

Koji Yamanoi, Tsukasa Baba, Kaoru Abiko, Junzo Hamanishi, Ken Yamaguchi, Ryusuke Murakami, Mana Taki, Yuko Hosoe, Susan K Murphy, Ikuo Konishi and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-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

12 citing papers in PubMed, 21 citations in OpenAlex.

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  12. Bioinformatics Identification of Key Genes for the Development and Prognosis of Lung Adenocarcinoma.Inquiry : a journal of medical care organization, provision and financing
    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

12 authors at 2 institutions in 2 countries.

Koji YamanoiDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.ORCID http://orcid.org/0000-0002-1240-5422
Tsukasa BabaDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.ORCID http://orcid.org/0000-0003-0066-3747
Kaoru AbikoDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Junzo HamanishiDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Ken YamaguchiDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.ORCID http://orcid.org/0000-0002-7669-1405
Ryusuke MurakamiDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Mana TakiDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yuko HosoeDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Susan K MurphyDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, Duke University Medical Center, Durham, USA.
Ikuo KonishiDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Masaki MandaiDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Noriomi MatsumuraDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan. noriomi@med.kindai.ac.jp.
Kyoto University · JPDuke Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Side population (SP) cells harbor malignant phenotypes in cancer. The aim of this study was to identify genes that modulate the proportion of ovarian cancer SP cells. Using a shRNA library targeting 15,000 genes, a functional genomics screen was performed to identify genes whose suppression increased the SP percentage. The biological effects caused by alteration of those identified genes were investigated in vitro and in vivo. We found that suppression of MSL3, ZNF691, VPS45, ITGB3BP, TLE2, and ZNF498 increased the proportion of SP cells. Newly generated SP cells exhibit greater capacity for sphere formation, single cell clonogenicity, and in vivo tumorigenicity. On the contrary, overexpression of MSL3, VPS45, ITGB3BP, TLE2, and ZNF498 decreased the proportion of SP cells, sphere formation capacity and single cell clonogenicity. In ovarian cancer cases, low expression of MSL3, ZNF691 and VPS45 was related to poor prognosis. Suppression of these six genes enhanced activity of the hedgehog pathway. Cyclopamine, a hedgehog pathway inhibitor, significantly decreased the number of SP cells and their sphere forming ability. Our results provide new information regarding molecular mechanisms favoring SP cells and suggest that Hedgehog signaling may provide a viable target for ovarian cancer.

Indexed as

Antineoplastic AgentsCell Line, TumorCell ShapeClone CellsDown-RegulationFemaleGene Expression Regulation, NeoplasticGene LibraryGenes, NeoplasmHedgehog ProteinsHumansInhibitory Concentration 50Kaplan-Meier EstimateOvarian NeoplasmsPhenotypePrognosisAntineoplastic AgentsHedgehog ProteinsRNA, MessengerRNA, NeoplasmRNA, Small Interfering

Identifiers

PMID31578411
PMCPMC6775117
OpenAlexW2977625049

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.