Evidence map›Paper›PMID 27081855›Full record

ArticlePloS one2016

Genome-Wide CRISPR-Cas9 Screen Identifies MicroRNAs That Regulate Myeloid Leukemia Cell Growth.

Jared Wallace, Ruozhen Hu, Timothy L Mosbruger, Timothy J Dahlem, W Zac Stephens, Dinesh S Rao, June L Round, Ryan M O'Connell

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
4.5field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
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  14. Article
  15. CRISPR in cancer biology and therapy.Nature reviews. Cancer · 2022
    Review
  16. Gene editing and its applications in biomedicine.Science China. Life sciences · 2022
    Review
  17. A new era in functional genomics screens.Nature reviews. Genetics · 2022
    Review
  18. Article
  19. Article
  20. Review
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 1 country.

Jared WallaceDepartment of Pathology, University of Utah, Salt Lake City, Utah, United States of America.
Ruozhen HuDepartment of Pathology, University of Utah, Salt Lake City, Utah, United States of America.
Timothy L MosbrugerHuntsman Cancer Institute, University of Utah, Salt Lake City, Utah, United States of America.
Timothy J DahlemMutation Generation and Detection Core, HSC Core Research Facilities, University of Utah, Salt Lake City, Utah, United States of America.
W Zac StephensDepartment of Pathology, University of Utah, Salt Lake City, Utah, United States of America.
Dinesh S RaoDepartment of Pathology, UCLA, Los Angeles, California, United States of America.
June L RoundDepartment of Pathology, University of Utah, Salt Lake City, Utah, United States of America.
Ryan M O'ConnellDepartment of Pathology, University of Utah, Salt Lake City, Utah, United States of America.
University of Utah · USHuntsman Cancer Institute · USUniversity of California, Los Angeles · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
Utilizing TALEN technology to regulate human microRNA'sDP2GM111099 · NIGMS · UNIVERSITY OF UTAH · PI O'CONNELL, RYAN M · 2013 to 2013
$2.2M
NCCDPHP CDC HHS DP2GM111099-01NCI NIH HHS 5P30CA042014-24NCI NIH HHS P30 CA042014NIGMS NIH HHS DP2 GM111099
6 · The paper itself

Abstract

Mammalian microRNA expression is dysregulated in human cancer. However, the functional relevance of many microRNAs in the context of tumor biology remains unclear. Using CRISPR-Cas9 technology, we performed a global loss-of-function screen to simultaneously test the functions of individual microRNAs and protein-coding genes during the growth of a myeloid leukemia cell line. This approach identified evolutionarily conserved human microRNAs that suppress or promote cell growth, revealing that microRNAs are extensively integrated into the molecular networks that control tumor cell physiology. miR-155 was identified as a top microRNA candidate promoting cellular fitness, which we confirmed with two distinct miR-155-targeting CRISPR-Cas9 lentiviral constructs. Further, we performed anti-correlation functional profiling to predict relevant microRNA-tumor suppressor gene or microRNA-oncogene interactions in these cells. This analysis identified miR-150 targeting of p53, a connection that was experimentally validated. Taken together, our study describes a powerful genetic approach by which the function of individual microRNAs can be assessed on a global level, and its use will rapidly advance our understanding of how microRNAs contribute to human disease.

Indexed as

CRISPR-Cas SystemsGenomicsAnimalsBase SequenceCell Line, TumorCell ProliferationConserved SequenceEvolution, MolecularHumansLeukemia, MyeloidMiceMicroRNAsMolecular Sequence DataTumor Suppressor Protein p53MicroRNAsTumor Suppressor Protein p53

Identifiers

PMID27081855
PMCPMC4833428
OpenAlexW2341542390

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.