Evidence map›Paper›PMID 31104397›Full record

ArticleIranian biomedical journal2019

BIRC5 Gene Disruption via CRISPR/Cas9n Platform Suppress Acute Myelocytic Leukemia Progression

Manizheh Narimani, Mohammadreza Sharifi, Mohammad Saeed Hakhamaneshi, Daem Roshani, Mohammad Kazemi, Seyed Hossein Hejazi, Ali Jalili

Open access · diamondAbstract read
In one paragraph

Article in Iranian biomedical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Visualization Analysis of CRISPR Gene-editing Knowledge Map based on Citespace.Biology bulletin of the Russian Academy of Sciences · 2021
    Article
  7. Article
  8. Article
  9. Knockout OfBlood and lymphatic cancer : targets and therapy · 2019
    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

7 authors at 2 institutions in 1 country.

Manizheh NarimaniCancer and Immunology Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Mohammadreza SharifiDepartment of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Mohammad Saeed HakhamaneshiCancer and Immunology Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Daem RoshaniCancer and Immunology Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Mohammad KazemiDepartment of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Seyed Hossein HejaziSkin Diseases and Leishmaniasis Research Center, Department of Parasitology & Mycology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Ali JaliliCancer and Immunology Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Kurdistan University of Medical Sciences · IRIsfahan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Acute myelocytic leukemia (AML) is a clonal malignancy resulting from the accumulation of genetic abnormalities in the cells. Human baculoviral inhibitor of apoptosis repeat-containing 5 (BIRC5), encodes survivin, is one of only a handful of genes that is differentially over-expressed in numerous malignant diseases including AML. Methods: The BIRC5 was silenced permanently in two AML cell lines, HL‑60 and KG-1, via the CRISPR/Cas9n system. After transfection of CRISPR constructs, genomic DNA was extracted and amplified to assess mutation detection. To evaluate BIRC5 gene expression, quantitative real-time PCR was performed. Also, MTT cell viability and Annexin‑V/propidium iodide flowcytometric staining were performed, and the data were analyzed using the Kolmogorov-Smirnov, Levene's, and ANOVA tests. Results: The results indicated that Cas9n and its sgRNAs successfully triggered site-specific cleavage and mutation in the BIRC5 gene locus. Moreover, suppression of BIRC5 resulted in the reduction of cell viability, and induction of apoptosis and necrosis in HL60 and KG1 suggested that the permanent suppression of BIRC5 remarkably dropped the gene expression and cells viability. Conclusion: This study reinforces the idea that BIRC5 disruption via Cas9n:sgRNAs has favorable effects on the AML clinical outcome. It thereby can be a promising candidate in a variety of leukemia treatments.

Indexed as

Disease ProgressionGene DeletionApoptosisBase SequenceCell Line, TumorCell ProliferationCell SurvivalCRISPR-Associated Protein 9CRISPR-Cas SystemsGene Expression Regulation, LeukemicHumansLeukemia, Myeloid, AcuteRNA, Guide, CRISPR-Cas SystemsSurvivinBIRC5 protein, humanCRISPR-Associated Protein 9RNA, Guide, CRISPR-Cas SystemsSurvivinAcute myelocytic leukemiaCRISPRGene editingSurvivin

Identifiers

PMID31104397
PMCPMC6800533
OpenAlexW2946418391

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.