Evidence map›Paper›PMID 33911969›Full record

ArticleSaudi journal of biological sciences2021

MicroRNA-567 inhibits cell proliferation and induces cell apoptosis in A549 NSCLC cells by regulating cyclin-dependent kinase 8.

Mohamed A Elkady, Ahmed S Doghish, Ahmed Elshafei, Mostafa M Elshafey

Open access · hybridAbstract read
In one paragraph

Article in Saudi journal of biological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

14 citing papers in PubMed, 85 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

4 authors at 2 institutions in 1 country.

Mohamed A ElkadyDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy (Boys), Al-Azhar University, Nasr City, Cairo 11651, Egypt.
Ahmed S DoghishDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy (Boys), Al-Azhar University, Nasr City, Cairo 11651, Egypt.
Ahmed ElshafeiDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy (Boys), Al-Azhar University, Nasr City, Cairo 11651, Egypt.
Mostafa M ElshafeyDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy (Boys), Al-Azhar University, Nasr City, Cairo 11651, Egypt.
Al-Azhar University · EGBadr University in Cairo · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA-567 (miR-567) plays a decisive role in cancers whereas its role in non-small cell lung cancer (NSCLC) is still unexplored. This study was therefore planned to explore the regulatory function of miR-567 in A549 NSCLC cells and investigate its possible molecular mechanism that may help in NSCLC treatment. In the current study, miR-567 expression was examined by quantitative real time-polymerase chain reaction (qRT-PCR) in different NSCLC cell lines in addition to normal cell line. A549 NSCLC cells were transfected by miR-567 mimic, miR-567 inhibitor, and negative control siRNA. Cell proliferation was evaluated by MTT and 5-bromo-2'deoxyuridine assays. Cell cycle distribution and apoptosis were studied by flow cytometry. Bioinformatics analysis programs were used to expect the putative target of miR-567. The expression of cyclin-dependent kinase 8 (CDK8) gene at mRNA and protein levels were evaluated by using qRT-PCR and western blotting. Our results found that miR-567 expressions decreased in all the studied NSCLC cells as compared to the normal cell line. A549 cell proliferation was suppressed by miR-567 upregulation while cell apoptosis was promoted. Also, miR-567 upregulation induced cell cycle arrest at sub-G1 and S phases. CDK8 was expected as a target gene of miR-567. MiR-567 upregulation decreased CDK8 mRNA and protein expression while the downregulation of miR-567 increased CDK8 gene expression. These findings revealed that miR-567 may be a tumor suppressor in A549 NSCLC cells through regulating CDK8 gene expression and may serve as a novel therapeutic target for NSCLC treatment.

Indexed as

16HBE, Normal human bronchial epithelial cell lineApoptosisATCC, American type culture collectionBrdU, 5-bromo- 2′-deoxyuridineCDK8CDK8, Cyclin-dependent kinase 8cDNA, Complementary DNACell cycleCell proliferationDAPI, 4′, 6-Diamidino-2 Phenylindole, DihydrochlorideDMEM, Dulbecco’s modified Eagle’s mediumDMSO, Dimethyl sulfoxideFBS, fetal bovine serumFITC, Fluorescein isothiocyanateh, HourLC, Lung cancerMiR-567MiR or MiRNA, MicroRNAmRNA, Messenger RNAMTT, 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromideNSCLCNSCLC, Non-small cell lung cancerPBS, phosphate buffer salinePI, Propidium iodidePVDF, Poly-vinylidene fluorideqRT-PCR, Quantitative real time-polymerase chain reactionRIPA, Radio immunoprecipitation assay

Identifiers

PMID33911969
PMCPMC8071907
OpenAlexW3132027627

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.