Evidence map›Paper›PMID 27323405›Full record

ArticleOncotarget2016

Suppression of ABHD2, identified through a functional genomics screen, causes anoikis resistance, chemoresistance and poor prognosis in ovarian cancer.

Koji Yamanoi, Noriomi Matsumura, Susan K Murphy, Tsukasa Baba, Kaoru Abiko, Junzo Hamanishi, Ken Yamaguchi, Masafumi Koshiyama, Ikuo Konishi, Masaki Mandai

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. 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
1.3field-weighted citation impact, top 21% 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, 38 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

10 authors at 3 institutions in 2 countries.

Koji YamanoiDepartment 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.
Susan K MurphyDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, Duke University Medical Center, Durham, NC, USA.
Tsukasa BabaDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
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.
Masafumi KoshiyamaDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Ikuo KonishiDepartment of Gynecology and Obstetrics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Masaki MandaiDepartment of Obstetrics and Gynecology, Faculty of Medicine, KinKi University, Osaka, Japan.
Kyoto University · JPDuke Medical Center · USKindai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anoikis resistance is a hallmark of cancer, and relates to malignant phenotypes, including chemoresistance, cancer stem like phenotypes and dissemination. The aim of this study was to identify key factors contributing to anoikis resistance in ovarian cancer using a functional genomics screen. A library of 81 000 shRNAs targeting 15 000 genes was transduced into OVCA420 cells, followed by incubation in soft agar and colony selection. We found shRNAs directed to ABHD2, ELAC2 and CYB5R3 caused reproducible anoikis resistance. These three genes are deleted in many serous ovarian cancers according to The Cancer Genome Atlas data. Suppression of ABHD2 in OVCA420 cells increased phosphorylated p38 and ERK, platinum resistance, and side population cells (p<0.01, respectively). Conversely, overexpression of ABHD2 decreased resistance to anoikis (p<0.05) and the amount of phosphorylated p38 and ERK in OVCA420 and SKOV3 cells. In clinical serous ovarian cancer specimens, low expression of ABHD2 was associated with platinum resistance and poor prognosis (p<0.05, respectively). In conclusion, we found three novel genes relevant to anoikis resistance in ovarian cancer using a functional genomics screen. Suppression of ABHD2 may promote a malignant phenotype and poor prognosis for women with serous ovarian cancer.

Indexed as

AnoikisCell Line, TumorDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticGenomicsHumansHydrolasesMiddle AgedOvarian NeoplasmsPrognosisRNA, Small InterferingSignal TransductionABHD2 protein, humanHydrolasesRNA, Small Interferinganoikis resistancefunctional genomics screenovarian cancershRNA library

Identifiers

PMID27323405
PMCPMC5216966
OpenAlexW2430181225

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.