Evidence map›Paper›PMID 27797825›Full record

ArticleCarcinogenesis2017

MCM7 and its hosted miR-25, 93 and 106b cluster elicit YAP/TAZ oncogenic activity in lung cancer.

Federica Lo Sardo, Mattia Forcato, Andrea Sacconi, Valeria Capaci, Francesca Zanconato, Silvia Di Agostino, Giannino Del Sal, Pier Paolo Pandolfi, Sabrina Strano, Silvio Bicciato and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
4.2field-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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

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  17. An overview of signaling pathways regulating YAP/TAZ activity.Cellular and molecular life sciences : CMLS · 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

11 authors at 4 institutions in 2 countries.

Federica Lo Sardo
Mattia ForcatoDepartment of Life Sciences, Center for Genome Research, University of Modena and Reggio Emilia, via G. Campi 287, 41100 Modena, Italy.
Andrea Sacconi
Valeria CapaciLaboratorio Nazionale CIB (LNCIB), Area Science Park Padriciano 99, 34149, Trieste, Italy.
Francesca ZanconatoDepartment of Molecular Medicine, University of Padua School of Medicine, viale Colombo 3, 35126 Padua, Italy.
Silvia Di Agostino
Giannino Del SalLaboratorio Nazionale CIB (LNCIB), Area Science Park Padriciano 99, 34149, Trieste, Italy.
Pier Paolo PandolfiDivision of Genetics Beth Israel Deaconess Medical Center, CLS Building, Room 401 330 Brookline Avenue Boston, MA 02215, USA and.
Sabrina StranoMolecular Chemoprevention Group, Molecular Medicine Area Regina Elena National Cancer Institute, via Elio Chianesi 53 00144, Rome, Italy.
Silvio BicciatoDepartment of Life Sciences, Center for Genome Research, University of Modena and Reggio Emilia, via G. Campi 287, 41100 Modena, Italy.
Giovanni Blandino
AREA Science Park · ITUniversity of Modena and Reggio Emilia · ITBeth Israel Deaconess Medical Center · USUniversity of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the first cause of cancer death worldwide and the Hippo pathway transcriptional coactivators YAP/TAZ have a pro-oncogenic role in this context. In order to understand the mechanisms through which YAP/TAZ elicit their oncogenic role in different systems, many studies are focused on YAP/TAZ target genes involved in the regulation of cell proliferation/survival and migration. However, there is scarce evidence on the role of YAP/TAZ in microRNA regulation while there is increasing evidence supporting the role of microRNAs in the main oncogenic processes. Here, we showed that YAP/TAZ were able to regulate several microRNAs in non-small cell lung cancer (NSCLC) cell lines. In detail, we focused on a cluster of three oncogenic microRNAs (miR-25, 93 and 106b) hosted in the MCM7 gene that were overexpressed in lung tumors compared to normal tissues. In addition, similar behavior was observed in breast cancer and head and neck tumor casuistries, where they showed a prognostic role. In NSCLC cells, YAP/TAZ induced the transcription of the MCM7 gene and its hosted miRs, thereby promoting cell proliferation through the post-transcriptional inhibition of the p21 cell cycle regulator. Accordingly, p21 was maintained at low levels in lung tumors compared to normal tissues. Conversely, its expression was restored in NSCLC cells upon YAP/TAZ interference or upon treatment with the statin cerivastatin. In summary, we provide evidence for a novel mechanism of modulation supporting the protumorigenic functions of the YAP/TAZ factors through the modulation of a bioncogenic locus consisting of one gene and three hosted microRNAs.

Indexed as

AcyltransferasesAdaptor Proteins, Signal TransducingCarcinogenesisCarcinoma, Non-Small-Cell LungCell ProliferationGene Expression Regulation, NeoplasticHumansLung NeoplasmsMicroRNAsMinichromosome Maintenance Complex Component 7PhosphoproteinsTranscription FactorsTumor Cells, CulturedYAP-Signaling ProteinsAcyltransferasesAdaptor Proteins, Signal TransducingMCM7 protein, humanMicroRNAsMinichromosome Maintenance Complex Component 7MIRN106 microRNA, humanMIRN25 microRNA, humanMIRN93 microRNA, humanPhosphoproteinsTAFAZZIN protein, humanTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID27797825
PMCPMC6276925
OpenAlexW2539084544

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.