Evidence map›Paper›PMID 23422749›Full record

ArticleBlood2013

Overexpression of miR-155 causes expansion, arrest in terminal differentiation and functional activation of mouse natural killer cells.

Rossana Trotta, Li Chen, Stefan Costinean, Srirama Josyula, Bethany L Mundy-Bosse, David Ciarlariello, Charlene Mao, Edward L Briercheck, Kathleen K McConnell, Anjali Mishra and 3 more

Abstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

37 citing papers in PubMed, 66 citations in OpenAlex.

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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 1 institution in 1 country.

Rossana TrottaThe Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA. rossana.trotta@osumc.edu
Li Chen
Stefan Costinean
Srirama Josyula
Bethany L Mundy-Bosse
David Ciarlariello
Charlene Mao
Edward L Briercheck
Kathleen K McConnell
Anjali Mishra
Lianbo Yu
Carlo M Croce
Michael A Caligiuri
Comprehensive Blood & Cancer Center · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI WANCAI YANG · 1985 to 2026
$132.3M
Tissue CoreP01CA081534 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RASSENTI, LAURA Z · 2000 to 2016
$59.5M
TWO SIGNAL REQUIREMENT FOR NATURAL KILLER IMMUNITYP01CA095426 · NCI · OHIO STATE UNIVERSITY · PI CARSON, WILLIAM E. · 2002 to 2016
$29.6M
ONOCOLOGY TRAINING GRANTT32CA009338 · NCI · OHIO STATE UNIVERSITY · PI BYRD, JOHN C., POLLOCK, RAPHAEL E. · 1985 to 2018
$8.3M
IL-15--CHARACTERIZATION THROUGH EXPERIMENTAL IMMUNOLOGYR01CA068458 · NCI · ROSWELL PARK CANCER INSTITUTE · PI CALIGIURI, MICHAEL A, YU, JIANHUA · 1996 to 2019
$4.5M
Role of miR155 in LeukemogenesisR01CA124541 · NCI · OHIO STATE UNIVERSITY · PI CROCE, CARLO M · 2008 to 2012
$1.8M
IL-15 characterization through experimental immunologyR37CA068458 · NCI · OHIO STATE UNIVERSITY · PI CALIGIURI, MICHAEL A · 2010 to 2014
$1.4M
NCI NIH HHS CA124541NCI NIH HHS CA16058NCI NIH HHS CA68458NCI NIH HHS CA95426NCI NIH HHS P01 CA081534NCI NIH HHS P01 CA095426NCI NIH HHS P30 CA016058NCI NIH HHS R01 CA068458NCI NIH HHS R01 CA124541NCI NIH HHS R37 CA068458NCI NIH HHS T32 CA009338NCI NIH HHS T32-CA009338
6 · The paper itself

Abstract

It is known that microRNAs (miRs) are involved in lymphocyte development, homeostasis, activation, and occasionally malignant transformation. In this study, a miR-155 transgene (tg) was driven to be overexpressed off of the lck promoter in order to assess its effects on natural killer (NK) cell biology in vivo. miR-155 tg mice have an increase in NK-cell number with an excess of the CD11b(low)CD27(high) NK subset, indicative of a halt in terminal NK-cell differentiation that proved to be intrinsic to the cell itself. The increase in NK cells results, in part, from improved survival in medium alone and enhanced expansion with endogenous or exogenous interleukin 15. Phenotypic and functional data from miR-155 tg NK cells showed constitutive activation and enhanced target cell conjugation, resulting in more potent antitumor activity in vitro and improved survival of lymphoma-bearing mice in vivo when compared with wild type NK cells. The enhanced NK-cell survival, expansion, activation, and tumor control that result from overexpression of miR-155 in NK cells could be explained, in part, via diminished expression of the inositol phosphatase SHIP1 and increased activation of ERK and AKT kinases. Thus, the regulation of miR-155 is important for NK-cell development, homeostasis, and activation.

Indexed as

Up-RegulationAnimalsCell CountCell DifferentiationCell Line, TumorCells, CulturedCell SurvivalDown-RegulationInositol Polyphosphate 5-PhosphatasesInterferon-gammaInterleukin-15Killer Cells, NaturalLymphomaMAP Kinase Signaling SystemMiceMice, Inbred C57BLInositol Polyphosphate 5-PhosphatasesInpp5d protein, mouseInterferon-gammaInterleukin-15MicroRNAsMirn155 microRNA, mousePhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphoric Monoester HydrolasesProto-Oncogene Proteins c-akt

Identifiers

PMID23422749
PMCPMC3630828
OpenAlexW2048238271

What OpenQuestion holds

Textmetadata
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.