Evidence map›Paper›PMID 21487000›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Sulfiredoxin-Peroxiredoxin IV axis promotes human lung cancer progression through modulation of specific phosphokinase signaling.

Qiou Wei, Hong Jiang, Zhen Xiao, Alyson Baker, Matthew R Young, Timothy D Veenstra, Nancy H Colburn

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

70 citing papers in PubMed, 110 citations in OpenAlex.

  1. Article
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  3. CRL3Nature communications · 2024
    Article
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  5. Review
  6. Article
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  11. Review
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  13. Review
  14. The role and mechanism of TXNDC5 in diseases.European journal of medical research · 2022
    Review
  15. Article
  16. Article
  17. Article
  18. Hyperoxidation of Peroxiredoxins and Effects on Physiology ofAntioxidants (Basel, Switzerland) · 2021
    Article
  19. Article
  20. Article

10 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 1 country.

Qiou WeiLaboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA. weiqiou@mail.nih.gov
Hong Jiang
Zhen Xiao
Alyson Baker
Matthew R Young
Timothy D Veenstra
Nancy H Colburn
Center for Cancer Research · USNational Cancer Institute · USAnatechScience Applications International Corporation (United States) · US

Funding

The Role of AP-1 and Other Transcription Factors in Cancer Cause and PreventionZIABC010025 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI COLBURN, NANCY H. · 2009 to 2013
$2.7M
The Role of Sulfiredoxin in Tumorigenesis and Cancer Progression.R00CA149144 · NCI · UNIVERSITY OF KENTUCKY · PI WEI, QIOU · 2012 to 2014
$709k
CCR NIH HHS HHSN261200800001CCIHRIntramural NIH HHS Z99 CA999999NCI NIH HHS HHSN261200800001ENCI NIH HHS K99 CA149144NCI NIH HHS R00 CA149144
6 · The paper itself

Abstract

Oxidative stress is known to cause tumorigenesis through induction of DNA and lipid damage. It also promotes cancer progression through a largely unknown mechanism. Sulfiredoxin (Srx) is a novel oxidative stress-induced antioxidant protein whose function in tumorigenesis and cancer progression has not been well studied. We report that Srx is highly expressed in human lung cancer. Knockdown of Srx reduces anchorage-independent colony formation, cell migration, and invasion of human lung cancer cells. Srx preferentially interacts with Peroxiredoxin (Prx) IV relative to other Prxs due to its intrinsic higher binding affinity. Knockdown of Prx IV recapitulates the phenotypic changes of depleting Srx. Disruption or enhancement of the Srx-Prx IV axis leads respectively to reduction or acceleration of tumor growth and metastasis formation in vivo. Through identification and validation of the downstream mediators we unraveled the Srx-mediated signaling network that traverses AP-1-activating and other phosphokinase signaling cascades. Our work reveals that the Srx-Prx IV axis is critical for lung cancer maintenance and metastasis, suggesting that targeting the Srx-Prx IV axis may provide unique effective strategies for cancer prevention and treatment.

Indexed as

Cell Line, TumorGene Knockdown TechniquesHEK293 CellsHumansLung NeoplasmsNeoplasm InvasivenessNeoplasm MetastasisNeoplasm ProteinsOxidative StressOxidoreductases Acting on Sulfur Group DonorsPeroxiredoxinsPhosphotransferasesSignal TransductionTranscription Factor AP-1Neoplasm ProteinsOxidoreductases Acting on Sulfur Group DonorsPeroxiredoxinsPhosphotransferasesPRDX4 protein, humanSRXN1 protein, humanTranscription Factor AP-1

Identifiers

PMID21487000
PMCPMC3084097
OpenAlexW2064415817

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.