Evidence map›Paper›PMID 27551492›Full record

ArticleCell death discovery2016

A Bowman-Birk inhibitor induces apoptosis in human breast adenocarcinoma through mitochondrial impairment and oxidative damage following proteasome 20S inhibition.

A Mehdad, Giselle Xavier Reis, A A Souza, Jarg Barbosa, M M Ventura, S M de Freitas

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 49 citations in OpenAlex.

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  10. Protease Inhibitors from Plants as Therapeutic Agents- A Review.Plant foods for human nutrition (Dordrecht, Netherlands) · 2022
    Review
  11. Revisiting the Domestication Process of AfricanPlants (Basel, Switzerland) · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 2 countries.

A MehdadLaboratory of Molecular Biophysics, Institute of Biological Sciences, University of Brasilia , Brasilia, Brazil.
Giselle Xavier ReisFaculty of Medicine, Department of Molecular Pathology, University of Brasilia , Brasilia, Brazil.
A A SouzaLaboratory of Molecular Biophysics, Institute of Biological Sciences, University of Brasilia , Brasilia, Brazil.
Jarg BarbosaLaboratory of Molecular Biophysics, Institute of Biological Sciences, University of Brasilia , Brasilia, Brazil.
M M VenturaLaboratory of Molecular Biophysics, Institute of Biological Sciences, University of Brasilia , Brasilia, Brazil.
S M de FreitasLaboratory of Molecular Biophysics, Institute of Biological Sciences, University of Brasilia , Brasilia, Brazil.
Universidade de Brasília · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proteasome inhibitors are emerging as a new class of chemopreventive agents and have gained huge importance as potential pharmacological tools in breast cancer treatment. Improved understanding of the role played by proteases and their specific inhibitors in humans offers novel and challenging opportunities for preventive and therapeutic intervention. In this study, we demonstrated that the Bowman-Birk protease inhibitor from Vigna unguiculata seeds, named black-eyed pea trypsin/chymotrypsin Inhibitor (BTCI), potently suppresses human breast adenocarcinoma cell viability by inhibiting the activity of proteasome 20S. BTCI induced a negative growth effect against a panel of breast cancer cells, with a concomitant cytostatic effect at the G2/M phase of the cell cycle and an increase in apoptosis, as observed by an augmented number of cells at the sub-G1 phase and annexin V-fluorescin isothiocyanate (FITC)/propidium iodide (PI) staining. In contrast, BTCI exhibited no cytotoxic effect on normal mammary epithelial cells. Moreover, the increased levels of intracellular reactive oxygen species (ROS) and changes in the mitochondrial membrane potential in cells treated with BTCI indicated mitochondrial damage as a crucial cellular event responsible for the apoptotic process. The higher activity of caspase in tumoral cells treated with BTCI in comparison with untreated cells suggests that BTCI induces apoptosis in a caspase-dependent manner. BTCI affected NF-kB target gene expression in both non invasive and invasive breast cancer cell lines, with the effect highly pronounced in the invasive cells. An increased expression of interleukin-8 (IL-8) in both cell lines was also observed. Taken together, these results suggest that BTCI promotes apoptosis through ROS-induced mitochondrial damage following proteasome inhibition. These findings highlight the pharmacological potential and benefit of BTCI in breast cancer treatment.

Identifiers

PMID27551492
PMCPMC4979482
OpenAlexW2329733919

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.