Evidence map›Paper›PMID 36358931›Full record

ReviewBiomolecules2022

Metabolism of Selenium, Selenocysteine, and Selenoproteins in Ferroptosis in Solid Tumor Cancers.

Briana K Shimada, Sydonie Swanson, Pamela Toh, Lucia A Seale

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.9field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Selenium: A Key Element in Inflammatory Bowel Disease.Antioxidants (Basel, Switzerland) · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Zinc, copper, copper-to-zinc ratio, and other biometals in blood serum and tumor tissue of patients with colorectal cancer.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025
    Article
  14. Review
  15. Article
  16. Article
  17. Review
  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

4 authors at 1 institution in 1 country.

Briana K ShimadaPacific Biosciences Research Center, University of Hawaii at Manoa, Honolulu, HI 96822, USA.ORCID 0000-0003-1521-6966
Sydonie SwansonPacific Biosciences Research Center, University of Hawaii at Manoa, Honolulu, HI 96822, USA.
Pamela TohPacific Biosciences Research Center, University of Hawaii at Manoa, Honolulu, HI 96822, USA.
Lucia A SealePacific Biosciences Research Center, University of Hawaii at Manoa, Honolulu, HI 96822, USA.ORCID 0000-0002-0686-7516
University of Hawaiʻi at Mānoa · US

Funding

Selenium Metabolism in the Heart: Impact of High Fructose and Low SeleniumP20GM139753 · NIGMS · UNIVERSITY OF HAWAII AT MANOA · PI Marla J Berry · 2022 to 2026
$13.3M
Selenium metabolism in cold-induced adaptive thermogenesisR01DK128390 · NIDDK · UNIVERSITY OF HAWAII AT MANOA · PI SEALE, LUCIA ANDREIA · 2021 to 2025
$2.0M
NIDDK NIH HHS R01 DK128390NIDDK NIH HHS R01DK128390NIGMS NIH HHS P20 GM139753
6 · The paper itself

Abstract

A potential target of precision nutrition in cancer therapeutics is the micronutrient selenium (Se). Se is metabolized and incorporated as the amino acid selenocysteine (Sec) into 25 human selenoproteins, including glutathione peroxidases (GPXs) and thioredoxin reductases (TXNRDs), among others. Both the processes of Se and Sec metabolism for the production of selenoproteins and the action of selenoproteins are utilized by cancer cells from solid tumors as a protective mechanism against oxidative damage and to resist ferroptosis, an iron-dependent cell death mechanism. Protection against ferroptosis in cancer cells requires sustained production of the selenoprotein GPX4, which involves increasing the uptake of Se, potentially activating Se metabolic pathways such as the trans-selenation pathway and the TXNRD1-dependent decomposition of inorganic selenocompounds to sustain GPX4 synthesis. Additionally, endoplasmic reticulum-resident selenoproteins also affect apoptotic responses in the presence of selenocompounds. Selenoproteins may also help cancer cells adapting against increased oxidative damage and the challenges of a modified nutrient metabolism that result from the Warburg switch. Finally, cancer cells may also rewire the selenoprotein hierarchy and use Se-related machinery to prioritize selenoproteins that are essential to the adaptations against ferroptosis and oxidative damage. In this review, we discuss both the evidence and the gaps in knowledge on how cancer cells from solid tumors use Se, Sec, selenoproteins, and the Se-related machinery to promote their survival particularly via resistance to ferroptosis.

Indexed as

FerroptosisNeoplasmsSeleniumHumansSelenocysteineSelenoproteinsSeleniumSelenocysteineSelenoproteinscancerferroptosisseleniumselenium metabolismsolid tumors

Identifiers

PMID36358931
PMCPMC9687593
OpenAlexW4307947108

What OpenQuestion holds

Textmetadata
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.