Evidence map›Paper›PMID 31571107›Full record

ArticleMolecular biology reports2019

Evaluation of the CRISPR/Cas9 directed mutant TP53 gene repairing effect in human prostate cancer cell line PC-3.

Muhammet Burak Batır, Ergin Şahin, Fethi Sırrı Çam

Abstract read
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In one paragraph

Article in Molecular biology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Review
  2. Review
  3. Precision medicine in prostate cancer: individualized treatment through radiomics, genomics, and biomarkers.Cancer imaging : the official publication of the International Cancer Imaging Society · 2025
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Various Aspects of a Gene Editing System-CRISPR-Cas9.International journal of molecular sciences · 2020
    Review
  16. Review
  17. Review
  18. Article
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

3 authors.

Muhammet Burak BatırDepartment of Biology, Faculty of Science and Letters, Manisa Celal Bayar University, Manisa, Turkey. burak.batir@cbu.edu.tr.ORCID http://orcid.org/0000-0002-8722-5055
Ergin ŞahinDepartment of Biology, Faculty of Science, Ankara University, Ankara, Turkey.
Fethi Sırrı ÇamDepartment of Medical Genetics, Faculty of Medicine, Manisa Celal Bayar University, Manisa, Turkey.

Funding

Celal Bayar Üniversitesi FEF 2017-144
6 · The paper itself

Abstract

Prostate cancer is a common health problem among men worldwide and most of these prostate cancer cases are related to a dysfunctional mutant Tumor Protein p53 (TP53) gene. However, the CRISPR/Cas9 system can be used for repairing of a dysfunctional mutant TP53 gene in combination with donor single-stranded oligodeoxynucleotide (ssODN) via cells' own homology-directed repair (HDR) mechanism. In this study, we aimed to evaluate the CRISPR/Cas9 repairing efficiency on TP53 414delC (p.K139fs*31) null mutation, located in the TP53 gene, of human prostate cancer cell line PC-3 in combination with ssODNs. According to the next-generation sequencing results, TP53 414delC mutation was repaired with an efficiency of 19.95% and 26.0% at the TP53 414delC position with ssODN1 and ssODN2 accompanied by sgRNA2 guided CRISPR/Cas9, respectively. Besides, qPCR and immunofluorescence analysis showed that PC-3 cells, the TP53 414delC mutation of which were repaired, expressed wild type p53 again. Also, significantly increased number of apoptotic cells, driven by the repaired TP53 gene were detected compared to the control cells by flow cytometry analysis. As a result, sgRNA2 guided CRISPR/Cas9 system accompanied by ssODN was shown to effectively repair the TP53 414delC gene region and inhibit the cell proliferation of PC-3 cells. Therefore, the effects of the TP53 414delC mutation repairment in PC-3 cells will be investigated in the in vivo models for tumor clearance analysis in the near future.

Indexed as

CRISPR-Cas SystemsDNA RepairMutationApoptosisCell ProliferationDNA, Single-StrandedHigh-Throughput Nucleotide SequencingHumansMaleOligodeoxyribonucleotidesPC-3 CellsProstatic NeoplasmsRNA, Guide, CRISPR-Cas SystemsSequence Analysis, DNATumor Suppressor Protein p53DNA, Single-StrandedOligodeoxyribonucleotidesRNA, Guide, CRISPR-Cas SystemsTP53 protein, humanTumor Suppressor Protein p53CRISPR/Cas9Homology-directed repair (HDR)p53Prostate cancerTP53 gene

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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.