Evidence map›Paper›PMID 31554377›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2019

Targeting Epidermal Growth Factor Receptor by MiRNA-145 Inhibits Cell Growth and Sensitizes NSCLC Cells to Erlotinib.

Jamal Amri, Neda Molaee, Maryam Baazm, Hadi Karami

Open access · goldAbstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

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  7. The Features of Immune Checkpoint Gene Regulation by microRNA in Cancer.International journal of molecular sciences · 2022
    Review
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  9. Cell Behavior of Non-Small Cell Lung Cancer Is at EGFR and MicroRNAs Hands.International journal of molecular sciences · 2021
    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

4 authors at 1 institution in 1 country.

Jamal AmriMolecular and Medicine Research Center, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran.
Neda MolaeeDepartment of Molecular Medicine and Biotechnology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran. Email:h.karami@arakmu.ac.irORCID 0000-0001-5314-193X
Maryam BaazmDepartment of Anatomy, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran.
Hadi KaramiMolecular and Medicine Research Center, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran.ORCID 0000-0002-8824-8160
Arak University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Despite effective activity of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), such as erlotinib, all non-small cell lung cancer (NSCLC) patients eventually acquire resistance to these agents. Studies have demonstrated that down-regulation of miRNA-145 leads to enhancement of EGFR expression, cell proliferation and metastasis. The aim of this study was to investigate the effect of miRNA-145 on sensitivity of the A549 NSCLC cells to erlotinib. Methods: Quantitative real-time PCR was used to examine the effect of miRNA-145 on EGFR expression. The effect of miRNA-145 on cell growth and sensitivity the lung cancer cells to erlotinib was examined by trypan blue and MTT assays, respectively. The combination index was calculated using the non-constant method of Chou-Talalay. Apoptosis was determined by ELISA cell death assay. Results: We found that miRNA-145 was markedly suppressed the expression of EGFR and inhibited the cancer cell growth, relative to blank control and negative control miRNA (p<0.05). Pretreatment with miRNA-145 synergistically enhanced the sensitivity of the lung cancer cells to erlotinib. Results of apoptosis assay revealed that miRNA-145 can induce apoptosis and increase the erlotinib-mediated apoptosis. Conclusions: Our data demonstrate that miRNA-145 play a critical role in the lung cancer cell growth, survival and EGFR-TKIs resistance possibly by regulation of EGFR. Therefore, miRNA-145 replacement therapy can become a new therapeutic strategy in lung cancer.

Indexed as

Antineoplastic AgentsApoptosisCarcinoma, Non-Small-Cell LungCell CycleCell ProliferationDrug Resistance, NeoplasmErbB ReceptorsErlotinib HydrochlorideGene Expression Regulation, NeoplasticHumansLung NeoplasmsMicroRNAsTumor Cells, CulturedAntineoplastic AgentsEGFR protein, humanErbB ReceptorsErlotinib HydrochlorideMicroRNAsMIRN145 microRNA, humanApoptosisgrowthLung cancerMiRNA-145tyrosine kinase inhibitor

Identifiers

PMID31554377
PMCPMC6976848
OpenAlexW2975046929

What OpenQuestion holds

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LicenceCC BY
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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.