Evidence map›Paper›PMID 31675930›Full record

ArticleBMC cancer2019

Suppression of nicotinamide phosphoribosyltransferase expression by miR-154 reduces the viability of breast cancer cells and increases their susceptibility to doxorubicin.

Zahra Bolandghamat Pour, Mitra Nourbakhsh, Kazem Mousavizadeh, Zahra Madjd, Seyedeh Sara Ghorbanhosseini, Zohreh Abdolvahabi, Zahra Hesari, Samira Ezzati Mobasser

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

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  15. CTRP13 Mitigates Abdominal Aortic Aneurysm Formation via NAMPT1.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
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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

8 authors at 4 institutions in 1 country.

Zahra Bolandghamat PourDepartment of Molecular Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Hemmat Highway 1449614535, Tehran, Iran.
Mitra NourbakhshDepartment of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. nourbakhsh.m@iums.ac.ir.ORCID http://orcid.org/0000-0002-6716-0354
Kazem MousavizadehDepartment of Molecular Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Hemmat Highway 1449614535, Tehran, Iran. mousavizadeh.k@iums.ac.ir.
Zahra MadjdDepartment of Molecular Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Hemmat Highway 1449614535, Tehran, Iran.
Seyedeh Sara GhorbanhosseiniDepartment of Biochemistry, Faculty of Pharmacy, Isfahan University of Medical Sciences, Isfahan, Iran.
Zohreh AbdolvahabiDepartment of Biochemistry and Genetics, Cellular and Molecular Research Center, Qazvin University of Medical Sciences, Qazvin, Iran.
Zahra HesariLaboratory Sciences Research Center, Golestan University of Medical Sciences, Gorgan, Iran.
Samira Ezzati MobasserDepartment of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Iran University of Medical Sciences · IRGolestan University · IRIsfahan University of Medical Sciences · IRQazvin University of Medical Sciences · IR

Funding

Iran University of Medical Sciences 27355
6 · The paper itself

Abstract

backgroundNicotinamide phosphoribosyltransferase (NAMPT) enzyme acts as the major enzyme in the nicotinamide adenine dinucleotide (NAD) synthesis salvage pathway. Deregulation of NAD could be associated with progression of several cancers such as breast cancer. Here, the consequence of NAMPT inhibition by miR-154 was investigated on breast cancer cells.

methodsMDA-MB-231 and MCF-7 cancer cell lines were transfected with the mimic and inhibitors of miR-154-5p and their corresponding negative controls. Consequently, levels of NAMPT and NAD were assayed employing qRT-PCR, Western blotting and enzymatic method, respectively. Subsequently, flow cytometry and colorimetric methods were performed to evaluate apoptosis and cell viability. Bioinformatics analyses as well as luciferase assay were done to investigate whether the 3'-UTR of NAMPT is directly targeted by miR-154.

resultsAccording to the obtained results, NAMPT was recognized as a target for binding of miR-154 and the levels of this miRNA was inversely associated with both mRNA and protein levels of NAMPT in breast cancer cell lines. Functionally, miR-154 inhibited the NAD salvage pathway leading to a remarkable decrease in cell viability and increased rate of cell death. When breast cancer cells were simultaneously treated with doxorubicin and miR-154 mimic, cell viability was considerably reduced compared to treatment with doxorubicin alone in both cell lines.

conclusionsIt was concluded that the inhibition of NAD production by miR-154 might be introduced as an appropriate therapeutic approach in order to improve breast cancer outcome either alone or in combination with other conventional chemotherapeutic agents.

Indexed as

3' Untranslated RegionsAntineoplastic Agents, AlkylatingApoptosisBreast NeoplasmsCell SurvivalComputational BiologyDoxorubicinDrug Resistance, NeoplasmEnzyme ActivationFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMicroRNAsNicotinamide Phosphoribosyltransferase3' Untranslated RegionsAntineoplastic Agents, AlkylatingDoxorubicinMicroRNAsMIRN154 microRNA, humanNicotinamide PhosphoribosyltransferaseBreast cancerDoxorubicinmicroRNAmiR-154Nicotinamide phosphoribosyltransferase

Identifiers

PMID31675930
PMCPMC6824125
OpenAlexW2988232833

What OpenQuestion holds

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LicenceCC BY
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.