Evidence map›Paper›PMID 24904997›Full record

ArticlePloS one2014

Proteomic analysis of bladder cancer indicates Prx-I as a key molecule in BI-TK/GCV treatment system.

Li Jiang, Xiao Xiao, Jin Ren, YongYong Tang, HongQing Weng, Qi Yang, MingJun Wu, Wei Tang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.7field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. International journal of molecular sciences · 2023
    Article
  4. Review
  5. Review
  6. Review
  7. Membrane Bound Peroxiredoxin-1 Serves as a Biomarker forAntioxidants & redox signaling · 2022
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Peroxiredoxin 1 - an antioxidant enzyme in cancer.Journal of cellular and molecular medicine · 2017
    Review
  14. Review
  15. Article
  16. Article
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 2 institutions in 1 country.

Li JiangDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Xiao XiaoDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jin RenDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
YongYong TangDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
HongQing WengDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Qi YangDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
MingJun WuInstitute of Life Science, Chongqing Medical University, Chongqing, China.
Wei TangDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In order to understand the molecular mechanisms of Bifidobacterium infantis thymidine kinase/nucleoside analogue ganciclovir (BI-TK/GCV) treatment system which was proven to exhibit sustainable anti-tumor growth activity and induce apoptosis in bladder cancer, a proteomic approach of isobaric tags for relative and absolute quantification (iTRAQ), followed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used. 192 down-regulated and 210 up-regulated proteins were identified after treatment with BI-TK/GCV system in Sprague-Dawley (SD) rats. Western blot analysis and immunohistochemistry analysis confirmed that Peroxiredoxin-I (Prx-I) was significantly down-regulated in bladder cancer after treatment. Prx-I silencing by transfection of Prx-I shRNA significantly suppressed growth, promoted apoptosis and regulated the cell cycle in T24 cells and reduced the phospho-NF-κB p50 and p65 protein expression which revealed the links between Prx-I and NF-κB pathway implied by Ingenuity pathway analysis (IPA). These findings yield new insights into the therapy of bladder cancer, revealing Prx-I as a new therapeutic target and indicating BI-TK/GCV system as a prospective therapy by down-regulation of Prx-I through NF-κB signaling pathway.

Indexed as

ProteomicsAnimalsApoptosisBifidobacteriumCell CycleCell ProliferationDown-RegulationFemaleGanciclovirGene Knockdown TechniquesGenetic TherapyNF-kappa BPeroxiredoxinsRatsRats, Sprague-DawleySignal TransductionGanciclovirNF-kappa BPeroxiredoxinsThymidine Kinase

Identifiers

PMID24904997
PMCPMC4048271
OpenAlexW1985964328

What OpenQuestion holds

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LicenceCC BY
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.