Evidence map›Paper›PMID 27364574›Full record

ArticleCancer gene therapy2016

Locked nucleic acid anti-miR-21 inhibits cell growth and invasive behaviors of a colorectal adenocarcinoma cell line: LNA-anti-miR as a novel approach.

R Nedaeinia, M Sharifi, A Avan, M Kazemi, L Rafiee, M Ghayour-Mobarhan, R Salehi

Abstract read
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In one paragraph

Article in Cancer gene therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.9field-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

43 citing papers in PubMed, 77 citations in OpenAlex.

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  17. miRNAs in Cancer (Review of Literature).International journal of molecular sciences · 2022
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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 1 country.

R NedaeiniaDepartment of Medical Biotechnology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
M SharifiDepartment of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.ORCID 0000-0002-1538-9034
A AvanMolecular Medicine Group, Department of Modern Sciences and Technologies, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
M KazemiDepartment of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
L RafieeApplied Physiology Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
M Ghayour-MobarhanMolecular Medicine Group, Department of Modern Sciences and Technologies, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
R SalehiDepartment of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Isfahan University of Medical Sciences · IRMashhad University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is the third leading cause of cancer-related death and has an extremely poor prognosis. Dysregulation of microRNAs (miRNAs) has been shown to be involved in the pathogenesis and progression of many malignancies. Recent data suggest that microRNA-21 (miR-21) is significantly elevated in different types of cancer, especially colon adenocarcinoma. Against this background, locked nucleic acid (LNA)-modified oligonucleotides have recently been suggested as a novel approach for targeting miRNAs as antisense-based gene silencing. The aim of the current study was to explore the functional role of LNA-anti-miR-21 in a colon adenocarcinoma LS174T cell line. LS174T cells were transfected with LNA-anti-miR-21 for 24, 48 and 72 h. Quantitative real-time reverse transcriptase-PCR (qRT-PCR) was performed to assess miR-21 expression by LNA-anti-miR-21. The viability of the cells was evaluated by MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide) assay and Annexin V/propidium iodide staining assay was used to detect apoptosis. Moreover, invasive behavior of the cells was evaluated before and after therapy by transwell assay. LNA-anti-miR-21 was successfully transfected in human LS174T cells and suppressed the endogenous miR-21. LNA-anti-miR-21 inhibited the cells' growth followed by induction of apoptosis. LNA-anti-miR-21 (50 pmol/μl) reduced the invasive behaviors of LS174T cells after 24 h, compared with untreated cells and scrambled LNA-transfected cells. However, this effect was more pronounced after 72 h. Our findings suggest the therapeutic potential of LNA-anti-miR-21 in a colon adenocarcinoma for targeting miR-21 expression. Further studies are warranted to investigate the molecular mechanisms underlying this novel inhibitor in colorectal cancer to establish its potential value for treatment of CRC patients with high miR-21 expression.

Indexed as

AdenocarcinomaApoptosisCell Line, TumorCell MovementCell ProliferationCell SurvivalColorectal NeoplasmsGene ExpressionGene Expression RegulationHumansMicroRNAsOligonucleotidesRNA, Antisenselocked nucleic acidMicroRNAsMIRN21 microRNA, humanOligonucleotidesRNA, Antisense

Identifiers

PMID27364574
OpenAlexW2472175394

What OpenQuestion holds

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Read underepoch 390

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.