Evidence map›Paper›PMID 23027624›Full record

ArticleCarcinogenesis2012

Superoxide dismutase 3 is induced by antioxidants, inhibits oxidative DNA damage and is associated with inhibition of estrogen-induced breast cancer.

Bhupendra Singh, Hari K Bhat

Abstract read
In one paragraph

Article in Carcinogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

57 citing papers in PubMed, 107 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The Potential of Superoxide Dismutase-RichInternational journal of molecular sciences · 2025
    Review
  9. Article
  10. Article
  11. Overexpression of Extracellular Superoxide Dismutase 3 Inhibits Cancer Cell Growth and Migration in Colorectal Cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
    Article
  12. Review
  13. Article
  14. Article
  15. Copper in the tumor microenvironment and tumor metastasis.Journal of clinical biochemistry and nutrition · 2022
    Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Effects of neoadjuvant therapies on genetic regulation of targeted pathways in ER+ primary ductal breast carcinoma: A meta-analysis of microarray datasets.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2021
    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

2 authors at 1 institution in 1 country.

Bhupendra SinghDivision of Pharmacology and Toxicology, School of Pharmacy, University of Missouri-Kansas City, 2464 Charlotte Street, Room 5251, Kansas City, MO 64108, USA.
Hari K Bhat
University of Missouri–Kansas City · US

Funding

Molecular Mechanisms & Importance of Oxidative Stress in Estrogen-Induced CarcinoR01CA109551 · NCI · UNIVERSITY OF MISSOURI KANSAS CITY · PI BHAT, HARI K · 2006 to 2011
$1.1M
NCI NIH HHS CA 109551
6 · The paper itself

Abstract

Epidemiological data and studies in rodent models strongly support the role of estrogens in the development of breast cancers. Oxidative stress has been implicated in this carcinogenic process. We have recently demonstrated that antioxidants vitamin C or butylated hydroxyanisole (BHA) severely inhibit 17β-estradiol (E2)-induced breast tumor development in female ACI rats. The objective of this study was to characterize the mechanism of antioxidant-mediated prevention of breast cancer. Female August Copenhagen Irish (ACI) rats were treated with E2, vitamin C, vitamin C + E2, BHA and BHA + E2 for up to 8 months. Superoxide dismutase 3 (SOD3) was suppressed in E2-exposed mammary tissues and in mammary tumors of rats treated with E2. This suppression was overcome by co-treatment of rats with E2 and vitamin C or BHA. 8-Hydroxydeoxyguanosine (8-OHdG) levels determined as a marker of oxidative DNA damage were higher in E2-exposed mammary tissues and in mammary tumors compared with age-matched controls. Vitamin C or BHA treatment significantly decreased E2-mediated increase in 8-OHdG levels in the mammary tissues and in MCF-10A cells. Increased DNA damage, colony and mammosphere formation, and migration in SOD3 knocked down MCF-10A cells, and nuclear translocation of SOD3 in vitamin C-treated mammary tissues and in MCF-10A cells suggest protective role of SOD3 against DNA damage and mammary carcinogenesis. Our studies further demonstrate that SOD3, but not SOD2 and SOD1, is induced by antioxidants and is regulated through NRF2. SOD3 may thus be an important gene in defense against oxidative stress and in the prevention of estrogen-mediated breast cancer.

Indexed as

DNA DamageActive Transport, Cell NucleusAntioxidantsAscorbic AcidBreast NeoplasmsButylated HydroxyanisoleCell Line, TumorEstradiolFemaleGene Expression Regulation, EnzymologicHumansNF-E2-Related Factor 2RNA, MessengerSuperoxide DismutaseSuperoxide Dismutase-1Superoxide Dismutase 2AntioxidantsAscorbic AcidButylated HydroxyanisoleEstradiolNFE2L2 protein, humanNF-E2-Related Factor 2RNA, MessengerSOD1 protein, humanSod1 protein, ratSOD3 protein, humanSuperoxide DismutaseSuperoxide Dismutase-1Superoxide Dismutase 2

Identifiers

PMID23027624
PMCPMC3510741
OpenAlexW2100590284

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.