Evidence map›Paper›PMID 29212257›Full record

ArticleOncotarget2017

Lentiviral CRISPR/Cas9 nickase vector mediated BIRC5 editing inhibits epithelial to mesenchymal transition in ovarian cancer cells.

Guannan Zhao, Qinghui Wang, Qingqing Gu, Wenan Qiang, Jian-Jun Wei, Peixin Dong, Hidemichi Watari, Wei Li, Junming Yue

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
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  3. Survivin targeting triple-fusion vaccineMedical oncology (Northwood, London, England) · 2025
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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

9 authors at 4 institutions in 2 countries.

Guannan ZhaoDepartment of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, USA.
Qinghui WangDepartment of Pharmaceutical Sciences, University of Tennessee Health Science Center, Memphis, USA.
Qingqing GuDepartment of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, USA.
Wenan QiangDepartment of Pathology, Department of Obstetrics and Gynecology, Northwestern University School of Medicine, Chicago, USA.
Jian-Jun WeiDepartment of Pathology, Department of Obstetrics and Gynecology, Northwestern University School of Medicine, Chicago, USA.
Peixin DongDepartment of Women's Health Educational System, Hokkaido University School of Medicine, Hokkaido University, Sapporo, Japan.
Hidemichi WatariDepartment of Women's Health Educational System, Hokkaido University School of Medicine, Hokkaido University, Sapporo, Japan.
Wei LiDepartment of Pharmaceutical Sciences, University of Tennessee Health Science Center, Memphis, USA.
Junming YueDepartment of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, USA.
University of Tennessee Health Science Center · USHokkaido University · JPNorthwestern University · USCenter for Cancer Research · US

Funding

Spatio-Temporal Organization of Chromatin and Information Transfer in CancerU54CA193419 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BACKMAN, VADIM · 2015 to 2020
$10.4M
Selective Targeting Survivin for Cancer TherapyR01CA193609 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LI, WEI · 2016 to 2020
$1.9M
NCI NIH HHS R01 CA193609NCI NIH HHS U54 CA193419
6 · The paper itself

Abstract

BIRC5 encodes the protein survivin, a member of the inhibitor of apoptosis family. Survivin is highly expressed in a variety of cancers but has very low expression in the corresponding normal tissues, and its expression is often associated with tumor metastasis and chemoresistance. We report that survivin was highly expressed in ovarian cancer and strongly correlated with patient overall poor survival. For the first time, we provide experimental evidence that survivin is involved in epithelial to mesenchymal transition (EMT) in ovarian cancer cells. Lentiviral CRISPR/Cas9 nickase vector mediated BIRC5 gene editing led to the inhibition of EMT by upregulating epithelial cell marker, cytokeratin 7 and downregulating mesenchymal markers: snail2, β-catenin, and vimentin in both ovarian cancer SKOV3 and OVCAR3 cells. Consistent with this molecular approach, pharmacological treatment of ovarian cancer cells using a small molecule survivin inhibitor, YM155 also inhibited EMT in these ovarian cancer cell lines. Overexpression of BIRC5 promoted EMT in SKOV3 cells. Using molecular or pharmacological approaches, we found that cell proliferation, migration, and invasion were significantly inhibited following BIRC5 disruption in both cell lines. Inhibition of BIRC5 expression also sensitized cell responses to paclitaxel treatment. Moreover, loss of BIRC5 expression attenuated TGFβ signaling in both SKOV3 and OVCAR3 cells. Collectively, our studies demonstrated that disruption of BIRC5 expression inhibited EMT by attenuating the TGFβ pathway in ovarian cancer cells.

Indexed as

BIRC5 (survivin)CRISPR/Cas9 nickaseepithelial to mesenchymal transitionlentiviral vectorovarian cancer

Identifiers

PMID29212257
PMCPMC5706903
OpenAlexW2767139158

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.