Evidence map›Paper›PMID 28918907›Full record

ReviewBiomedical journal2017

Thioredoxin promotes survival signaling events under nitrosative/oxidative stress associated with cancer development.

Hugo P Monteiro, Fernando T Ogata, Arnold Stern

Open access · goldAbstract readReview
In one paragraph

Review in Biomedical journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 18% 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, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. The Importance of Thioredoxin-1 in Health and Disease.Antioxidants (Basel, Switzerland) · 2023
    Review
  12. Article
  13. Article
  14. Review
  15. Deciphering the Path ofAntioxidants (Basel, Switzerland) · 2022
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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

3 authors at 3 institutions in 3 countries.

Hugo P MonteiroDepartment of Biochemistry, Center for Cellular and Molecular Therapy - CTCMol, Paulista Medical School/Federal University of São Paulo, SP, Brazil.
Fernando T OgataDepartment of Biochemistry, Center for Cellular and Molecular Therapy - CTCMol, Paulista Medical School/Federal University of São Paulo, SP, Brazil; Division of Biochemistry, Medical Biochemistry & Biophysics, Karolinska Institutet, Stockholm, Sweden.
Arnold SternNew York University School of Medicine, New York, NY, USA. Electronic address: arnold.stern@nyumc.org.
Karolinska Institutet · SENew York University · USUniversidade Federal de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating mutations may drive cells into the acquisition of abnormal phenotypes that are characteristic of cancer cells. Cancer cells feature profound alterations in proliferation programs that result in a new population of cells that overrides normal tissue construction and maintenance programs. To achieve this goal, cancer cells are endowed with up regulated survival signaling pathways. They also must counteract the cytotoxic effects of high levels of nitric oxide (NO) and of reactive oxygen species (ROS), which are by products of cancer cell growth. Accumulating experimental evidence associates cancer cell survival with their capacity to up-regulate antioxidant systems. Elevated expression of the antioxidant protein thioredoxin-1 (Trx1) has been correlated with cancer development. Trx1 has been characterized as a multifunctional protein, playing different roles in different cell compartments. Trx1 migrates to the nucleus in cells exposed to nitrosative/oxidative stress conditions. Trx1 nuclear migration has been related to the activation of transcription factors associated with cell survival and cell proliferation. There is a direct association between the p21Ras-ERK1/2 MAP Kinases survival signaling pathway and Trx1 nuclear migration under nitrosative stress. The expression of the cytoplasmic protein, the thioredoxin-interacting protein (Txnip), determines the change in Trx1 cellular compartmentalization. The anti-apoptotic actions of Trx1 and its denitrosylase activity occur in the cytoplasm and serve as important regulators of cell survival. Within this context, this review focuses on the participation of Trx1 in cells under nitrosative/oxidative stress in survival signaling pathways associated with cancer development.

Indexed as

AntioxidantsCell SurvivalHumansNeoplasmsOxidation-ReductionOxidative StressThioredoxinsAntioxidantsThioredoxinsCancer developmentDenitrosylationNitric oxideS-nitrosylationSurvival signalingThioredoxin-1

Identifiers

PMID28918907
PMCPMC6136292
OpenAlexW2740951267

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.