Evidence map›Paper›PMID 31942196›Full record

ArticleJournal of Cancer2020

The Nucleolin Antagonist N6L Inhibits LINE1 Retrotransposon Activity in Non-Small Cell Lung Carcinoma Cells.

Kenneth S Ramos, Sara Moore, Isabel Runge, Marco A Tavera-Garcia, Ilaria Cascone, Jose Courty, Elsa M Reyes-Reyes

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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, 1 synthesis or guideline pooled it, 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

7 authors at 2 institutions in 2 countries.

Kenneth S RamosTexas A&M University College of Medicine, Department of Medicine and Institute of Biosciences and Technology, Houston, Texas 77030, USA.
Sara MooreUniversity of Arizona College of Medicine, Department of Medicine, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Tucson, Arizona 85721.
Isabel RungeUniversity of Arizona College of Medicine, Department of Medicine, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Tucson, Arizona 85721.
Marco A Tavera-GarciaUniversity of Arizona College of Medicine, Department of Medicine, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Tucson, Arizona 85721.
Ilaria CasconeUniversity of Paris Est (UPEC), ERL-CNRS 9215, Laboratory of Growth, Reparation, and Tissue Regeneration (CRRET), UPEC, 94010 Créteil, France.
Jose CourtyUniversity of Paris Est (UPEC), ERL-CNRS 9215, Laboratory of Growth, Reparation, and Tissue Regeneration (CRRET), UPEC, 94010 Créteil, France.
Elsa M Reyes-ReyesUniversity of Arizona College of Medicine, Department of Medicine, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Tucson, Arizona 85721.
University of Arizona · USLaboratoire de Recherche sur la Croissance Cellulaire, la Réparation et la Régénération Tissulaires · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the most common cause of cancer death in the United States. The genome of non-small cell lung cancer (NSCLC), the most frequent lung cancer type, is strongly affected by Long Interspersed Nuclear Element (LINE1) insertions. Active LINE1s are repetitive DNA sequences that can amplify themselves in the genome utilizing a retrotransposition mechanism whereby LINE1 is copied via reverse transcription and inserted at target sites. ORF1p and ORF2p are LINE1 encoded proteins essential for LINE1 retrotransposition. LINE1s are silenced epigenetically in somatic tissues, and their reactivation has been associated with cancer pathogenesis. Here, we present evidence that nucleolin (NCL) regulates expression of LINE1-ORF1p (L1-ORF1p) in NSCLC cells. Genetic knockdown of NCL significantly inhibited expression of L1-ORF1p in various NSCLC cell lines. Treatment with the investigational NCL antagonist N6L ablated L1-ORF1p expression in all cell lines constitutively expressing L1-ORFp. N6L displayed a stronger antiproliferative activity in NSCLC tumor cell lines expressing the highest L1-ORF1p protein levels. Moreover, N6L treatment of nude mice bearing NSCLC tumor xenografts blocked L1-ORF1p expression and effectively inhibited tumor growth

Indexed as

and Lung cancer.LINE1NSCLCNucleolin

Identifiers

PMID31942196
PMCPMC6959038
OpenAlexW3005674612

What OpenQuestion holds

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LicenceCC BY
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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.