Evidence map›Paper›PMID 27480083›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2016

A network including PU.1, Vav1 and miR-142-3p sustains ATRA-induced differentiation of acute promyelocytic leukemia cells - a short report.

Silvia Grassilli, Ervin Nika, Elisabetta Lambertini, Federica Brugnoli, Roberta Piva, Silvano Capitani, Valeria Bertagnolo

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2016. 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
1.9field-weighted citation impact, top 14% 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, 16 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

7 authors at 1 institution in 1 country.

Silvia GrassilliSection of Anatomy and Histology, Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, 44121, Ferrara, Italy.
Ervin NikaSection of Anatomy and Histology, Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, 44121, Ferrara, Italy.
Elisabetta LambertiniDepartment of Biomedical and Specialty Surgical Sciences, University of Ferrara, 44121, Ferrara, Italy.
Federica BrugnoliSection of Anatomy and Histology, Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, 44121, Ferrara, Italy.
Roberta PivaDepartment of Biomedical and Specialty Surgical Sciences, University of Ferrara, 44121, Ferrara, Italy.
Silvano CapitaniSection of Anatomy and Histology, Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, 44121, Ferrara, Italy.
Valeria BertagnoloSection of Anatomy and Histology, Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, 44121, Ferrara, Italy. bgv@unife.it.
University of Ferrara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeReduced expression of miR-142-3p has been found to be associated with the development of various subtypes of myeloid leukemia, including acute promyelocytic leukemia (APL). In APL-derived cells, miR-142-3p expression can be restored by all-trans retinoic acid (ATRA), which induces the completion of their maturation program. Here, we aimed to assess whether PU.1, essential for ATRA-induced gene transcription, regulates the expression of miR-142-3p in APL-derived cells and, based on the established cooperation between PU.1 and Vav1 in modulating gene expression, to evaluate the role of Vav1 in restoring the expression of miR-142-3p.

methodsATRA-induced increases in PU.1 and Vav1 expression in APL-derived NB4 cells were counteracted with specific siRNAs, and the expression of miR-142-3p was measured by quantitative real-time PCR (qRT-PCR). The recruitment of PU.1 and/or Vav1 to the regulatory region of miR-142 was assessed by quantitative chromatin immunoprecipitation (Q-ChIP). Synthetic inhibitors or mimics for miR-142-3p were used to assess whether this miRNA plays a role in regulating the expression of PU.1 and/or Vav1.

resultsWe found that the expression of miR-142-3p in differentiating APL-derived NB4 cells is dependent on PU.1, and that Vav1 is essential for the recruitment of this transcription factor to its cis-binding element on the miR-142 promoter. In addition, we found that in ATRA-treated NB4 cells miR-142-3p sustains agonist-induced increases in both PU.1 and Vav1.

conclusionsOur results suggest the existence of a Vav1/PU.1/miR-142-3p network that supports ATRA-induced differentiation in APL-derived cells. Since selective regulation of miRNAs may play a role in the future treatment of hematopoietic malignancies, our results may provide a basis for the development of new therapeutic strategies to restore the expression of miR-142-3p.

Indexed as

Antineoplastic AgentsCell DifferentiationCell Line, TumorChromatin ImmunoprecipitationGene Expression Regulation, LeukemicGene Knockdown TechniquesHumansLeukemia, Promyelocytic, AcuteMicroRNAsProto-Oncogene ProteinsProto-Oncogene Proteins c-vavProto-Oncogene Protein Spi-1Real-Time Polymerase Chain ReactionTrans-ActivatorsTretinoinAntineoplastic AgentsMicroRNAsMIRN142 microRNA, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-vavProto-Oncogene Protein Spi-1Trans-ActivatorsTretinoinVAV1 protein, humanAcute promyelocytic leukemiaATRAmiR-142-3pPU.1Vav1

Identifiers

PMID27480083
PMCPMC13001866
OpenAlexW2495119656

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.