Evidence map›Paper›PMID 35803440›Full record

ReviewFree radical biology & medicine2022

The beginning of GPX2 and 30 years later.

R Steven Esworthy, James H Doroshow, Fong-Fong Chu

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Selenium and Selenoproteins in Neutrophil Functions.Biological trace element research · 2026
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Cells · 2025
    Article
  15. Article
  16. TNFAIP8L2 maintains hair cell function and regulates age-related hearing loss via mTORC1 signaling.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  17. Article
  18. Article
  19. Review
  20. 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

3 authors at 2 institutions in 1 country.

R Steven EsworthyDepartment of Cancer Genetics & Epigenetics, Beckman Research Institute of City of Hope. Duarte, California, USA, 91010. Electronic address: sesworthy@coh.org.
James H DoroshowDivision of Cancer Treatment and Diagnosis, National Cancer Institute, NIH, Bethesda, MD, USA. Electronic address: doroshoj@mail.nih.gov.
Fong-Fong ChuDepartment of Cancer Genetics & Epigenetics, Beckman Research Institute of City of Hope. Duarte, California, USA, 91010. Electronic address: ffchu@coh.org.
Beckman Research InstituteNational Cancer Institute · US

Funding

The role of glutathione peroxidase in the pathogenesis of intestinal cancerR01CA114569 · NCI · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI CHU, FONG-FONG · 2006 to 2010
$1.4M
CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001ENCI NIH HHS R01 CA114569
6 · The paper itself

Abstract

We published the first paper to characterize GPX2 (aka GSHPx-GI) as a selenoenzyme with glutathione peroxidase activity in 1993. Among the four Se-GPX isozymes, GPX1-4, GPX1 and GPX2 are closely related in terms of structure, substrate specificities, and subcellular localization. What sets them apart are distinct patterns of gene regulation, tissue distribution and response to selenium. While we identified the digestive tract epithelium as the main site of GPX2 expression, later work has shown GPX2 is found more widely in epithelial tissues with concentration of expression in stem cell and proliferative compartments. GPX2 expression is regulated over a wide range of levels by many pathways, including NRF2, WNT, p53, RARE and this often results in attaching undue significance to GPX2 as GPX2 is only a part of a system of hydroperoxidase activities, including GPX1, peroxiredoxins and catalase. These other activities may play equal or greater roles, particularly in cell lines cultured without selenium supplementation and often with very low GPX2 levels. This could be assessed by examining levels of mRNA and protein among these various peroxidases at the outset of studies. As an example, it was found that GPX1 responds to the absence of GPX2 in mouse ileum and colon epithelium with higher expression. As such, both Gpx1 and Gpx2 had to be knocked out in mice to produce ileocolitis. However, we note that the actual role of GPX1 and GPX2 in relation to peroxiredoxin function is unclear. There may be an interdependence that requires only low amounts of GPX1 and/or GPX2 in a supporting role to maintain proper peroxiredoxin function. GPX2 levels may be prognostic for cancer progression in colon, breast, prostate and liver, however, there is no consistent trend for higher or lower levels to be favorable.

Indexed as

SeleniumAnimalsColonGlutathione PeroxidaseMaleMiceMice, Inbred C57BLMice, KnockoutPeroxiredoxinsGlutathione PeroxidasePeroxiredoxinsSeleniumGene regulationGPX1GPX2Knockout miceOxidative stressProliferative cellsSeleniumStem cells

Identifiers

PMID35803440
PMCPMC9341242
OpenAlexW4284704766

What OpenQuestion holds

Textmetadata
LicenceTDM
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.