Evidence map›Paper›PMID 33827661›Full record

ArticleCell & bioscience2021

EIF5A2 controls ovarian tumor growth and metastasis by promoting epithelial to mesenchymal transition via the TGFβ pathway.

Guannan Zhao, Wenjing Zhang, Peixin Dong, Hidemichi Watari, Yuqi Guo, Lawrence M Pfeffer, Gabor Tigyi, Junming Yue

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 28 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 4 institutions in 3 countries.

Guannan ZhaoDepartment of Pathology and Laboratory Medicine, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Wenjing ZhangDepartment of Genetics, Genomics & Informatics, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Peixin DongDepartment of Obstetrics and Gynecology, Hokkaido University Graduate School of Medicine, Sapporo, 060-8638, Japan.
Hidemichi WatariDepartment of Obstetrics and Gynecology, Hokkaido University Graduate School of Medicine, Sapporo, 060-8638, Japan.
Yuqi GuoPeople's Hospital of Zhengzhou University, Zhengzhou, Henan, China. yuqi-guo@163.com.
Lawrence M PfefferDepartment of Pathology and Laboratory Medicine, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Gabor TigyiDepartment of Physiology, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Junming YueDepartment of Pathology and Laboratory Medicine, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN, 38163, USA. jyue@uthsc.edu.
University of Tennessee Health Science Center · USHokkaido University · JPCenter for Cancer Research · USZhengzhou University · CN

Funding

Role of MTF1 in ovarian cancerR21CA216585 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI YUE, JUNMING · 2018 to 2019
$385k
NCI NIH HHS 1R21CA216585-01A1NCI NIH HHS R21 CA216585
6 · The paper itself

Abstract

backgroundEpithelial to mesenchymal transition (EMT) contributes to tumor metastasis and chemoresistance. Eukaryotic initiation factor 5A2 (EIF5A2) is highly expressed in a variety of human cancers but rarely expressed in normal tissues. While EIF5A2 has oncogenic activity in several cancers and contributes to tumor metastasis, its role in ovarian cancer is unknown. In this study, we investigate whether EIF5A2 contributes to ovarian tumor metastasis by promoting EMT.

methodsTo investigate the role of EIF5A2, we knocked out (KO) EIF5A2 using lentiviral CRISPR/Cas9 nickase in high invasive SKOV3 and OVCAR8 cells and overexpressed EIF5A2 in low invasive OVCAR3 cells using lentiviral vector. Cell proliferation, migration and invasion was examined in vitro ovarian cancer cells and tumor metastasis was evaluated in vivo using orthotopic ovarian cancer mouse models.

resultsHere we report that EIF5A2 is highly expressed in ovarian cancers and associated with patient poor survival. Lentiviral CRISPR/Cas9 nickase vector mediated knockout (KO) of EIF5A2 inhibits epithelial to mesenchymal transition (EMT) in SKOV3 and OVCAR8 ovarian cancer cells that express high levels of EIF5A2. In contrast, overexpression of EIF5A2 promotes EMT in OVCAR3 epithelial adenocarcinoma cells that express relatively low EIF5A2 levels. KO of EIF5A2 in SKOV3 and OVCAR8 cells inhibits ovarian cancer cell migration and invasion, while its overexpression promotes cell migration and invasion in OVCAR3 adenocarcinoma cells. We further demonstrate that EIF5A2 promotes EMT by activating the TGFβ pathway and KO of EIF5A2 inhibits ovarian tumor growth and metastasis in orthotopic ovarian cancer mouse models.

conclusionOur results indicate that EIF5A2 is an important controller of ovarian tumor growth and metastasis by promoting EMT and activating the TGFβ pathway.

Indexed as

Cas9 nickaseCRISPREIF5A2Epithelial to mesenchymal transitionLentiviral vectorOrthotopic ovarian cancer mouse modelOvarian cancer

Identifiers

PMID33827661
PMCPMC8025533
OpenAlexW3149873436

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.