Evidence map›Paper›PMID 28123598›Full record

ArticleJournal of Cancer2017

Lentiviral CRISPR/Cas9 vector mediated miR-21 gene editing inhibits the epithelial to mesenchymal transition in ovarian cancer cells.

Wenying Huo, Guannan Zhao, Jinggang Yin, Xuan Ouyang, Yinan Wang, Chuanhe Yang, Baojing Wang, Peixin Dong, Zhixiang Wang, Hidemichi Watari and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

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11 more citing papers are in PubMed but not listed here.

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

13 authors at 4 institutions in 3 countries.

Wenying HuoDepartment of Pathology and Laboratory Medicine; Center for Cancer Research; Department of Physiology; Henan Agricultural University; Henan University of Animal Husbandry and Economy, P.R. China.
Guannan ZhaoDepartment of Pathology and Laboratory Medicine; Center for Cancer Research.
Jinggang YinDepartment of Ophthalmology, University of Tennessee Health Science Center, Memphis, TN, USA.
Xuan OuyangDepartment of Pathology and Laboratory Medicine; Center for Cancer Research.
Yinan WangDepartment of Pathology and Laboratory Medicine; Center for Cancer Research.
Chuanhe YangDepartment of Pathology and Laboratory Medicine; Center for Cancer Research.
Baojing WangDepartment of Pathology and Laboratory Medicine; Center for Cancer Research.
Peixin DongDepartment of Women's Health Educational System.
Zhixiang WangHenan Agricultural University.
Hidemichi WatariDepartment of Gynecology, Hokkaido University School of Medicine, Hokkaido University, Sapporo, Japan.
Edward ChaumDepartment of Ophthalmology, University of Tennessee Health Science Center, Memphis, TN, USA.
Lawrence M PfefferDepartment of Pathology and Laboratory Medicine; Center for Cancer Research.
Junming YueDepartment of Pathology and Laboratory Medicine; Center for Cancer Research.
Center for Cancer Research · USHenan Agricultural University · CNHokkaido University · JPUniversity of Tennessee Health Science Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats) mediated genome editing is a powerful approach for loss of function studies. Here we report that lentiviral CRISPR/Cas9 vectors are highly efficient in introducing mutations in the precursor miRNA sequence, thus leading to the loss of miRNA expression and function. We constructed four different lentiviral CRISPR/Cas9 vectors that target different regions of the precursor miR-21 sequence and found that these lentiviral CRISPR/Cas9 miR-21 gRNA vectors induced mutations in the precursor sequences as shown by DNA surveyor mutation assay and Sanger sequencing. Two miR-21 lentiviral CRISPR/Cas9 gRNA vectors were selected to probe miR-21 function in ovarian cancer SKOV3 and OVCAR3 cell lines. Our data demonstrate that disruption of pre-miR-21 sequences leads to reduced cell proliferation, migration and invasion. Moreover, CRISPR/Cas9-mediated miR-21 gene editing sensitizes both SKOV3 and OVCAR3 cells to chemotherapeutic drug treatment. Disruption of miR-21 leads to the inhibition of epithelial to mesenchymal transition (EMT) in both SKOV3 and OVCAR3 cells as evidenced by the upregulation of epithelial cell marker E-cadherin and downregulation of mesenchymal marker genes, vimentin and Snai2. The miR-21 target genes PDCD4 and SPRY2 were upregulated in cells transduced with miR-21gRNAs compared to controls. Our study indicates that lentiviral CRISPR/Cas9-mediated miRNA gene editing is an effective approach to address miRNA function, and disruption of miR-21 inhibits EMT in ovarian cancer cells.

Indexed as

CRISPR/Cas9EMT.lentiviral vectormiR-21ovarian cancer

Identifiers

PMID28123598
PMCPMC5264040
OpenAlexW2567455584

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.