Evidence map›Paper›PMID 28124991›Full record

ArticleInternational journal of molecular sciences2017

mir-660-p53-mir-486 Network: A New Key Regulatory Pathway in Lung Tumorigenesis.

Cristina Borzi, Linda Calzolari, Giovanni Centonze, Massimo Milione, Gabriella Sozzi, Orazio Fortunato

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Urinary biomarkers for lung cancer detection.The journal of liquid biopsy · 2026
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  7. APE1 controls DICER1 expression in NSCLC through miR-33a and miR-130b.Cellular and molecular life sciences : CMLS · 2022
    Article
  8. MicroRNA networks in FLT3-ITD acute myeloid leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  10. Review
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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

6 authors at 1 institution in 1 country.

Cristina BorziDepartment of Experimental Oncology and Molecular Medicine, Unit of Tumor Genomics, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy. cristina.borzi@istitutotumori.mi.it.
Linda CalzolariDepartment of Experimental Oncology and Molecular Medicine, Unit of Tumor Genomics, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy. linda.calzolari@istitutotumori.mi.it.
Giovanni CentonzeDepartment of Experimental Oncology and Molecular Medicine, Unit of Tumor Genomics, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy. giovanni.centonze@istitutotumori.mi.it.
Massimo MilioneDepartment of Pathology and Laboratory Medicine, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy. massimo.milione@istitutotumori.mi.it.
Gabriella SozziDepartment of Experimental Oncology and Molecular Medicine, Unit of Tumor Genomics, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy. gabriella.sozzi@istitutotumori.mi.it.
Orazio FortunatoDepartment of Experimental Oncology and Molecular Medicine, Unit of Tumor Genomics, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy. orazio.fortunato@istitutotumori.mi.it.
Fondazione IRCCS Istituto Nazionale dei Tumori · IT

Funding

Identifying non-coding RNAs for early detection and prevention of lung cancerU01CA166905 · NCI · OHIO STATE UNIVERSITY · PI CROCE, CARLO M, PASS, HARVEY IRA · 2013 to 2017
$4.5M
NCI NIH HHS U01 CA166905
6 · The paper itself

Abstract

Lung cancer is the most frequent cause of cancer-related death worldwide, with limited therapeutic options and rapid development of drug resistance. MicroRNAs, a class of small non-coding RNAs that control different physiological processes, have been associated with cancer development, as either oncomiRNAs or tumor-suppressor miRNAs. In the present study we investigated the interaction between mir-486-5p and mir-660-5p, two independent tumor-suppressor miRNAs, to assess their possible role and synergistic effect in lung cancer treatment. Our data show that mir-660-5p over-expression in A549 lung cancer cells induced a remarkable increase in mir-486-5p expression level and activity, detected as a reduction of its target gene, p85. mir-486-5p expression was confirmed by microRNA in situ hybridization. mir-660-5p modulated mir-486-5p through the silencing of Mouse Double Minute 2 (MDM2), one of its direct target, and then through p53 stimulation. This regulatory pathway was effective in A549, but not in H1299; therefore, only in the context of a functional p53 protein. Our findings support the conclusion that mir-486-5p is positively regulated by mir-660-5p in lung cancer cell lines, through the mir-660-MDM2-p53 pathway, making mir-660-5p even more interesting for its potential successful use in lung cancer therapy.

Indexed as

Gene Regulatory NetworksAntineoplastic AgentsCarcinogenesisCell Line, TumorDown-RegulationGene Expression Regulation, NeoplasticGene SilencingHumansLung NeoplasmsMicroRNAsProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53Antineoplastic AgentsMDM2 protein, humanMicroRNAsMIRN486 microRNA, humanMIRN660 microRNA, humanProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53lung cancermiRNAsp53

Identifiers

PMID28124991
PMCPMC5297851
OpenAlexW2580850592

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.