Evidence map›Paper›PMID 28391184›Full record

ArticleRedox biology2017

Thioredoxin 1 modulates apoptosis induced by bioactive compounds in prostate cancer cells.

Aida Rodriguez-Garcia, David Hevia, Juan C Mayo, Pedro Gonzalez-Menendez, Lucia Coppo, Jun Lu, Arne Holmgren, Rosa M Sainz

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  14. Thioredoxin-dependent system. Application of inhibitors.Journal of enzyme inhibition and medicinal chemistry · 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 3 institutions in 2 countries.

Aida Rodriguez-GarciaDepartamento de Morfologia y Biologia Celular, Biology Unit, Instituto Universitario de Oncologia del Principado de Asturias (IUOPA), Universidad de Oviedo, 33006 Oviedo, Asturias, Spain.
David HeviaDepartamento de Morfologia y Biologia Celular, Biology Unit, Instituto Universitario de Oncologia del Principado de Asturias (IUOPA), Universidad de Oviedo, 33006 Oviedo, Asturias, Spain; Research and Development Department, Bioquochem S.L., Parque Tecnológico de Asturias, 33428 Llanera, Asturias, Spain.
Juan C MayoDepartamento de Morfologia y Biologia Celular, Biology Unit, Instituto Universitario de Oncologia del Principado de Asturias (IUOPA), Universidad de Oviedo, 33006 Oviedo, Asturias, Spain.
Pedro Gonzalez-MenendezDepartamento de Morfologia y Biologia Celular, Biology Unit, Instituto Universitario de Oncologia del Principado de Asturias (IUOPA), Universidad de Oviedo, 33006 Oviedo, Asturias, Spain.
Lucia CoppoDivision of Biochemistry, Department of Medical Biochemistry and Biophysics, Karolisnka Institute, SE-17177 Stockholm, Sweden.
Jun LuDivision of Biochemistry, Department of Medical Biochemistry and Biophysics, Karolisnka Institute, SE-17177 Stockholm, Sweden.
Arne HolmgrenDivision of Biochemistry, Department of Medical Biochemistry and Biophysics, Karolisnka Institute, SE-17177 Stockholm, Sweden.
Rosa M SainzDepartamento de Morfologia y Biologia Celular, Biology Unit, Instituto Universitario de Oncologia del Principado de Asturias (IUOPA), Universidad de Oviedo, 33006 Oviedo, Asturias, Spain. Electronic address: sainzrosa@uniovi.es.
Karolinska Institutet · SEUniversidad de Oviedo · ESInstituto de Investigación Sanitaria del Principado de Asturias · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence suggests that natural bioactive compounds, alone or in combination with traditional chemotherapeutic agents, could be used as potential therapies to fight cancer. In this study, we employed four natural bioactive compounds (curcumin, resveratrol, melatonin, and silibinin) and studied their role in redox control and ability to promote apoptosis in androgen sensitive and insensitive prostate cancer cells. Here is shown that curcumin and resveratrol promote ROS production and induce apoptosis in LNCaP and PC-3. An increase in reactive species is a trigger event in curcumin-induced apoptosis and a consequence of resveratrol effects on other pathways within these cells. Moreover, here we demonstrated that these four compounds affect differently one of the main intracellular redox regulator, the thioredoxin system. Exposure to curcumin and resveratrol promoted TRX1 oxidation and altered its subcellular location. Furthermore, resveratrol diminished TRX1 levels in PC-3 cells and increased the expression of its inhibitor TXNIP. Conversly, melatonin and silibinin only worked as cytostatic agents, reducing ROS levels and showing preventive effects against TRX oxidation. All together, this work explores the effect of compounds currently tested as chemo-preventive agents in prostate cancer therapy, on the TRX1 redox state and function. Our work shows the importance that the TRX system might have within the differences found in their mechanisms of action. These bioactive compounds trigger different responses and affect ROS production and redox systems in prostate cancer cells, suggesting the key role that redox-related pathways might play in processes like differentiation or survival in prostate cancer.

Indexed as

ApoptosisCarrier ProteinsCell Line, TumorCell SurvivalCurcuminGene Expression Regulation, NeoplasticHumansMaleMelatoninProstatic NeoplasmsReactive Oxygen SpeciesResveratrolSilybinSilymarinStilbenesThioredoxinsCarrier ProteinsCurcuminMelatoninReactive Oxygen SpeciesResveratrolSilybinSilymarinStilbenesThioredoxinsTXNIP protein, humanTXN protein, humanApoptosisProstate cancerRedox signalingThioredoxinThioredoxin reductaseTXNIP

Identifiers

PMID28391184
PMCPMC5385622
OpenAlexW2602121406

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.