Evidence map›Paper›PMID 35015757›Full record

ArticlePloS one2022

Overexpression of ultraconserved region 83- induces lung cancer tumorigenesis.

Ivan Vannini, Manuela Ferracin, Francesco Fabbri, Muller Fabbri

Abstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
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  5. Review
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

4 authors.

Ivan VanniniBiosciences Laboratory, IRCCS Istituto Romagnolo per lo Studio dei Tumori (IRST) "Dino Amadori", Meldola, Italy.ORCID 0000-0002-9279-1801
Manuela FerracinDepartment of Experimental, Diagnostic and Specialty Medicine-DIMES, University of Bologna, Bologna, Italy.
Francesco FabbriBiosciences Laboratory, IRCCS Istituto Romagnolo per lo Studio dei Tumori (IRST) "Dino Amadori", Meldola, Italy.
Muller FabbriCenter for Cancer and Immunology Research, Children's National Hospital, Washington, DC, United States of America.

Funding

Role of microRNAs released by Tumor Associated Macrophages within Exosomes in the chemoresistance of NeuroblastomaR01CA215753 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI FABBRI, MULLER · 2017 to 2021
$1.7M
Clinical Significance and Mechanism of Action of Exosomal microRNAs in Neuroblastoma chemoresistanceR01CA219024 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI FABBRI, MULLER · 2018 to 2022
$1.7M
NCI NIH HHS R01 CA215753NCI NIH HHS R01 CA219024
6 · The paper itself

Abstract

The expression of non-coding RNAs (ncRNAs) is dysregulated in human cancers. The transcribed ultraconserved regions (T-UCRs) express long ncRNAs involved in human carcinogenesis. T-UCRs are non-coding genomic sequence that are 100% conserved across humans, rats and mice. Conservation of genomic sequences across species intrinsically implies an essential functional role and so we considered the expression of T-UCRs in lung cancer. Using a custom microarray we analyzed the global expression of T-UCRs. Among these T-UCRs, the greatest variation was observed for antisense ultraconserved element 83 (uc.83-), which was upregulated in human lung cancer tissues compared with adjacent non cancerous tissues. Even though uc.83- is located within the long intergenic non-protein coding RNA 1876 (LINC01876) gene, we found that the transcribed uc.83- is expressed independently of LINC01876 and was cloned as a 1143-bp RNA gene. In this study, functional analysis confirmed important effects of uc.83- on genes involved in cell growth of human cells. siRNA against uc.83- decreased the growth of lung cancer cells while the upregulation through a vector overexpressing the uc.83- RNA increased cell proliferation. We also show the oncogenic function of uc.83- is mediated by the phosphorylation of AKT and ERK 1/2, two important biomarkers of lung cancer cell proliferation. Based on our findings, inhibition against uc.83- could be a future therapeutic treatment for NSCLC to achieve simultaneous blockade of pathways involved in lung carcinogenesis.

Indexed as

CarcinogenesisCarcinoma, Non-Small-Cell LungCell Cycle CheckpointsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansLung NeoplasmsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphorylationProto-Oncogene Proteins c-aktRNA InterferenceRNA, Long NoncodingRNA, Small InterferingUp-RegulationMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-aktRNA, Long NoncodingRNA, Small Interfering

Identifiers

PMID35015757
PMCPMC8752010

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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.