Evidence map›Paper›PMID 26025667›Full record

ArticleNeoplasia (New York, N.Y.)2015

STAT1: A Novel Target of miR-150 and miR-223 Is Involved in the Proliferation of HTLV-I-Transformed and ATL Cells.

Ramona Moles, Marcia Bellon, Christophe Nicot

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
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  17. Role of Virus-Induced Host Cell Epigenetic Changes in Cancer.International journal of molecular sciences · 2021
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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

3 authors at 2 institutions in 1 country.

Ramona MolesDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, USA.
Marcia BellonDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, USA.
Christophe NicotDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, USA. Electronic address: cnicot@kumc.edu.
University of Kansas Medical Center · USUniversity of Kansas · US

Funding

Role of miR-124a in HTLV-I oncogenesisR21CA141386 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI NICOT, CHRISTOPHE P · 2011 to 2012
$359k
NCI NIH HHS CA141386NCI NIH HHS R21 CA141386
6 · The paper itself

Abstract

We have previously reported on the deregulation of cellular microRNAs involved in hematopoiesis and inflammation in human T-cell lymphotropic virus type 1 (HTLV-I)-transformed cells. In this study, we demonstrate that miR-150 and miR-223 specifically target the signal transducer and activator of transcription 1 (STAT1) 3' untranslated region, reducing STAT1 expression and dampening STAT1-dependent signaling in human T cells. The effects of miR-150 and miR-223 on endogenous STAT1 were confirmed using inducible cell lines. Our studies also showed that miR-150 expression is upregulated by interleukin-2 signaling in adult T cell leukemia/lymphoma (ATL) cells. HTLV-I-transformed and ATL-derived cells have reduced levels of miR150 and miR223 expression, which coincide with increased STAT1 expression and STAT1-dependent signaling. Knockdown of STAT1 by short hairpin RNA demonstrated that the constitutive activation of STAT1 is required for the continuous proliferation of HTLV-I-transformed cells. Our studies further demonstrate that increased expression of STAT1 in ATL cells is associated with higher levels of major histocompatibility complex class I expression. Previous studies have demonstrated that the pressure exerted by natural killer (NK) cells in vivo can edit leukemic tumor cells by forcing an increased expression of major histocompatibility complex class I to escape immune clearance. STAT1-expressing tumor cells produce more aggressive tumors because they cannot be eliminated by NK cells. Our results suggest that therapeutic approaches using combined targeting of STAT1 and MHC class I may be an effective approach to activate NK cell-mediated clearance of ATL tumor cells.

Indexed as

3' Untranslated RegionsBlotting, WesternCell Line, TumorCell ProliferationCell Transformation, ViralGene Expression Regulation, LeukemicHistocompatibility Antigens Class IHumansHuman T-lymphotropic virus 1Killer Cells, NaturalLeukemia-Lymphoma, Adult T-CellMicroRNAsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionSTAT1 Transcription FactorTransfection3' Untranslated RegionsHistocompatibility Antigens Class IMicroRNAsMIR150, humanMIR223, humanSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID26025667
PMCPMC4468372
OpenAlexW1908521476

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.