Evidence map›Paper›PMID 32948832›Full record

ArticleCancer gene therapy2021

miR-34c-3p targets CDK1 a synthetic lethality partner of KRAS in non-small cell lung cancer.

Francesco Palma, Alessandra Affinito, Silvia Nuzzo, Giuseppina Roscigno, Iolanda Scognamiglio, Francesco Ingenito, Lola Martinez, Monica Franzese, Mario Zanfardino, Andrea Soricelli and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer gene therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 23 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 7 institutions in 3 countries.

Francesco PalmaDepartment of Molecular Medicine and Medical Biotechnology, "Federico II" University of Naples, Naples, Italy.
Alessandra AffinitoPercuros BV, Zernikedreef 8, 2333 CL, Leiden, The Netherlands.
Silvia NuzzoIRCCS SDN, Naples, Italy.
Giuseppina RoscignoDepartment of Molecular Medicine and Medical Biotechnology, "Federico II" University of Naples, Naples, Italy.
Iolanda ScognamiglioDepartment of Molecular Medicine and Medical Biotechnology, "Federico II" University of Naples, Naples, Italy.
Francesco IngenitoDepartment of Molecular Medicine and Medical Biotechnology, "Federico II" University of Naples, Naples, Italy.
Lola MartinezFlow Cytometry Core Unit, Biotechnology Programme, Spanish National Cancer Research Centre (CNIO), E-28029, Madrid, Spain.
Monica FranzeseIRCCS SDN, Naples, Italy.ORCID http://orcid.org/0000-0002-6490-7694
Mario ZanfardinoIRCCS SDN, Naples, Italy.
Andrea SoricelliIRCCS SDN, Naples, Italy.ORCID http://orcid.org/0000-0001-7011-7667
Alfonso FiorelliThoracic Surgery Unit, Università degli Studi della Campania "Luigi Vanvitelli,", Naples, Italy.
Gerolama CondorelliDepartment of Molecular Medicine and Medical Biotechnology, "Federico II" University of Naples, Naples, Italy. gecondor@unina.it.ORCID http://orcid.org/0000-0003-0177-8829
Cristina QuintavalleInstitute of Experimental Endocrinology and Oncology (IEOS) G. Salvatore, CNR, Naples, Italy. cristina.quintavalle@ieos.cnr.it.
SDN Istituto di Ricerca Diagnostica e Nucleare · ITPercuros (Netherlands) · NLUniversity of Naples Federico II · ITFederico II University Hospital · ITInstitute for Experimental Endocrinology and Oncology · ITSpanish National Cancer Research Centre · ESUniversity of Campania "Luigi Vanvitelli" · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is still the leading cause of death by cancer worldwide despite advances both in its detection and therapy. Multiple oncogenic driver alterations have been discovered, opening the prospective for new potential therapeutic targets. Among them, KRAS mutations represent the most frequent oncogene aberrations in non-small cell lung cancer (NSCLC) patients with a negative prognostic impact, but effective therapies targeting KRAS are not well characterized yet. Here, we demonstrate that the microRNA miR-34c-3p is a positive prognostic factor in KRAS-mutated NSCLC patients. Firstly, looking at the TGCA dataset, we found that high miR-34c-3p expression correlated with longer survival of KRAS-mutated NSCLC patients. In vitro assays on immortalized and patient-derived primary NSCLC cells revealed that miR-34c-3p overexpression increased apoptosis and lowered proliferation rate in KRAS

Indexed as

Gene Expression Regulation, NeoplasticSynthetic Lethal MutationsAdenocarcinoma of LungApoptosisCarcinoma, Non-Small-Cell LungCDC2 Protein KinaseCell MovementCell ProliferationHumansLung NeoplasmsMicroRNAsPrognosisProspective StudiesProto-Oncogene Proteins p21(ras)Survival RateTumor Cells, CulturedCDC2 Protein KinaseCDK1 protein, humanKRAS protein, humanMicroRNAsMIRN34 microRNA, humanProto-Oncogene Proteins p21(ras)

Identifiers

PMID32948832
PMCPMC8119240
OpenAlexW3087296890

What OpenQuestion holds

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Registered trials

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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.