Evidence map›Paper›PMID 28152509›Full record

ArticleOncotarget2017

microRNA-210-3p depletion by CRISPR/Cas9 promoted tumorigenesis through revival of TWIST1 in renal cell carcinoma.

Hirofumi Yoshino, Masaya Yonemori, Kazutaka Miyamoto, Syuichi Tatarano, Satoshi Kofuji, Nijiro Nohata, Masayuki Nakagawa, Hideki Enokida

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 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
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  4. Review
  5. Article
  6. Review
  7. Targeted disruption of theActa biochimica et biophysica Sinica · 2024
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  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. CRISPR-Cas knockout of miR21 reduces glioma growth.Molecular therapy oncolytics · 2022
    Article
  15. Article
  16. Review
  17. The Role of MiRNA in Cancer: Pathogenesis, Diagnosis, and Treatment.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  18. Article
  19. Review
  20. Observational
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 3 institutions in 2 countries.

Hirofumi YoshinoDepartment of Urology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima 890-8520, Japan.
Masaya YonemoriDepartment of Urology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima 890-8520, Japan.
Kazutaka MiyamotoDepartment of Urology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima 890-8520, Japan.
Syuichi TataranoDepartment of Urology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima 890-8520, Japan.
Satoshi KofujiDepartment of Internal Medicine, Vontz Center, University of Cincinnati, College of Medicine, Ohio 45267-0508, USA.
Nijiro NohataMoores UCSD Cancer Center, La Jolla, CA 92093-0803, USA.
Masayuki NakagawaDepartment of Urology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima 890-8520, Japan.
Hideki EnokidaDepartment of Urology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima 890-8520, Japan.
Kagoshima University · JPMoores Cancer CenterUniversity of Cincinnati Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies showed that five miRNAs (miR-885-5p, miR-1274, miR-210-3p, miR-224 and miR-1290) were upregulated the most in clear cell renal cell carcinoma (ccRCC). Our focus was to understand from a clinical standpoint the functional consequences of upregulating miR-210-3p. Towards this, we utilized the CRISPR/Cas9 gene editing system to deplete miR-210-3p in RCC cell lines (786-o, A498 and Caki2) and characterized the outcomes. We observed that miR-210-3p depletion dramatically increased tumorigenesis, including altering the morphology of A498 and Caki2 cells in a manner characteristic of epithelial-mesenchymal transition (EMT). These results were corroborated by in vivo xenograft studies, which showed enhanced growth of tumors from miR-210-3p-depleted A498 cells. We identified Twist-related protein 1 (TWIST1) as a key target of miR-210-3p. Analysis of the ccRCC patient data in The Cancer Genome Atlas database showed a negative correlation between miR-210-3p and TWIST1 expression. High TWIST1 and low miR-210-3p expression associated with poorer overall and disease-free survival as compared to low TWIST1 and high miR-210-3p expression. These findings suggest that renal cell carcinoma progression is promoted by TWIST1 suppression mediated by miR-210-3p.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorCarcinoma, Renal CellCell MovementCell ProliferationCell Transformation, NeoplasticCRISPR-Cas SystemsEpithelial-Mesenchymal TransitionFemaleHumansKidney NeoplasmsMiceMice, Inbred BALB CMice, NudeBiomarkers, TumorMicroRNAsMIRN210 microRNA, humanNuclear ProteinsTWIST1 protein, humanTwist-Related Protein 1CRISPR/Cas9microRNAmiR-210-3prenal cell carcinomaTWIST1

Identifiers

PMID28152509
PMCPMC5400553
OpenAlexW2583954636

What OpenQuestion holds

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Registered trials

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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.