Evidence map›Paper›PMID 25232487›Full record

ArticleAmerican journal of cancer research2014

Expression of peroxiredoxin 1 and 4 promotes human lung cancer malignancy.

Hong Jiang, Lisha Wu, Murli Mishra, Hedy A Chawsheen, Qiou Wei

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing 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

41 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
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  8. Article
  9. Article
  10. Review
  11. MnTnHex-2-PyPAntioxidants (Basel, Switzerland) · 2022
    Article
  12. Review
  13. Membrane Bound Peroxiredoxin-1 Serves as a Biomarker forAntioxidants & redox signaling · 2022
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  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

5 authors at 1 institution in 1 country.

Hong JiangGraduate Center for Toxicology, University of Kentucky College of Medicine Lexington, KY 40536, USA ; The Markey Cancer Center, University of Kentucky College of Medicine Lexington, KY 40536, USA.
Lisha WuGraduate Center for Toxicology, University of Kentucky College of Medicine Lexington, KY 40536, USA ; The Markey Cancer Center, University of Kentucky College of Medicine Lexington, KY 40536, USA.
Murli MishraGraduate Center for Toxicology, University of Kentucky College of Medicine Lexington, KY 40536, USA ; The Markey Cancer Center, University of Kentucky College of Medicine Lexington, KY 40536, USA.
Hedy A ChawsheenGraduate Center for Toxicology, University of Kentucky College of Medicine Lexington, KY 40536, USA ; The Markey Cancer Center, University of Kentucky College of Medicine Lexington, KY 40536, USA.
Qiou WeiGraduate Center for Toxicology, University of Kentucky College of Medicine Lexington, KY 40536, USA ; The Markey Cancer Center, University of Kentucky College of Medicine Lexington, KY 40536, USA.
The Graduate Center, CUNY · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI Bernard Mark Evers · 2013 to 2026
$38.3M
Center for Biomedical Research Excellence in the Molecular Basis of Human DiseaseP20GM103486 · NIGMS · UNIVERSITY OF KENTUCKY · PI LOUIS HERSH, LOUIS HERSH LOUIS HERSH · 2012 to 2013
$4.2M
The Role of Sulfiredoxin in Tumorigenesis and Cancer Progression.R00CA149144 · NCI · UNIVERSITY OF KENTUCKY · PI WEI, QIOU · 2012 to 2014
$709k
NCI NIH HHS P30 CA177558NCI NIH HHS R00 CA149144NIGMS NIH HHS P20 GM103486
6 · The paper itself

Abstract

Members of the Peroxiredoxin (Prx) family are major cellular antioxidants that scavenge hydrogen peroxide and play essential roles in oxidative stress and cell signaling. 2-Cys Prxs, including Prx1, 2, 3 and 4, have been indicated in multiple oncogenic signaling pathways and thus may contribute to various processes of cancer development. The significance of 2-Cys Prxs in lung cancer development and their biological function in signal transduction have not been fully investigated. In this study we analyzed the expression of 2-Cys Prxs in lung cancer, and examined their levels of expression in a variety of cell lines established from human lung normal or cancer tissues. We found that 2-Cys Prxs, in particular, Prx1 and Prx4, were preferentially expressed in cell lines derived from human lung cancer. Through isoform specific knockdown of individual Prx, we demonstrated that Prx1 and Prx4 (but not Prx3) were required for human lung cancer A549 cells to form soft agar colony and to invade through matrigel in culture. Knockdown of Prx1 or Prx4 significantly reduced the activation of c-Jun and repressed the AP-1 mediated promoter activity. In mouse xenograft models, knockdown of Prx4 in A549 cells reduced subcutaneous tumor growth and blocked metastasis formation initiated through tail vein injection. Moreover, overexpression of Prx1 or Prx4 further enhanced the malignancy of A549 cells both in culture and in mouse xenografts in vivo. These data provide an in-depth understanding of the contribution of Prx1 and Prx4 to lung cancer development and are of importance for future development of therapeutic methods that targeting 2-Cys Prxs.

Indexed as

cell signalinglung cancerPeroxiredoxintumor invasion and metastasis

Identifiers

PMID25232487
PMCPMC4163610
OpenAlexW70692427

What OpenQuestion holds

Textmetadata
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.