Evidence map›Paper›PMID 29096636›Full record

ArticleLipids in health and disease2017

Sodium butyrate promotes apoptosis in breast cancer cells through reactive oxygen species (ROS) formation and mitochondrial impairment.

Vahid Salimi, Zahra Shahsavari, Banafsheh Safizadeh, Ameinh Hosseini, Narges Khademian, Masoumeh Tavakoli-Yaraki

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.

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25 more citing papers are in PubMed but not listed here.

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

6 authors at 4 institutions in 1 country.

Vahid SalimiDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Zahra ShahsavariDepartment of Laboratory Medicine, Faculty of Paramedical Sciences, Shaheed Beheshti University of Medical Sciences, Tehran, Iran.
Banafsheh SafizadehDepartment of Biochemistry, Faculty of Medicine, Birjand University of Medical Sciences, Birjand, Iran.
Ameinh HosseiniDepartment of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Narges KhademianDepartment of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Masoumeh Tavakoli-YarakiDepartment of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. tavakoli.m@iums.ac.ir.
Iran University of Medical Sciences · IRBirjand University of Medical Sciences · IRShahid Beheshti University of Medical Sciences · IRTehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSodium butyrate (NaBu) is a short-chain fatty acid which serves as a histon deacetylase inhibitor and has received considerable interest as a possible regulator of cancer cell death. The regulatory effect of NaBu on cancer cell growth or death has yet to be illustrated in many cancers including breast cancer. This study is aimed to elucidate the possible effect of NaBu on regulation of breast cancer growth and apoptosis.

methodsThe cytotoxic effect of NaBu on the growth of breast cancer cells (MCF-7 and MDA-MB-468) and normal breast cells (MCF-10A) was determined using MTT assay. Annexin-V-FITC staining and PI staining were performed to detect apoptosis and cell cycle distribution using Flow cytometry, the level of mitochondrial membrane potential (Δψm), Reactive oxygen species (ROS)formation and caspase activity were determined accordingly.

resultsBased on our data, NaBu induced a dose and time-dependent cell toxicity in breast cancer cells which was related to the cell cycle arrest and induction of apoptosis. The impact of NaBu on MCF-10A cell toxicity, cell cycle distribution and apoptosis was inconsiderable. NaBu-elicited apoptosis was accompanied by the elevated level of ROS, increased caspase activity and reduced mitochondrial membrane potential (Δψm) in MCF-7 and MDA-MB-468 cells and with no effect on the above mentioned factors in MCF-10A cells.

conclusionsOur study provided insight in to the role of NaBu on the regulation of breast cancer cell growth and lighten up the pro-apoptotic activity of NaBu.

Indexed as

Antineoplastic AgentsApoptosisButyric AcidCaspasesCell CycleCell LineCell Line, TumorCell ProliferationDose-Response Relationship, DrugEpithelial CellsFemaleHumansMammary Glands, HumanMCF-7 CellsMembrane Potential, MitochondrialMitochondriaAntineoplastic AgentsButyric AcidCaspasesReactive Oxygen SpeciesApoptosisCaspaseCell cycleMitochondrial membrane potential (Δψm)Reactive oxygen speciesSodium butyrate

Identifiers

PMID29096636
PMCPMC5669027
OpenAlexW2765113361

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.