Evidence map›Paper›PMID 24894866›Full record

ArticleCarcinogenesis2014

Resveratrol inhibits estrogen-induced breast carcinogenesis through induction of NRF2-mediated protective pathways.

Bhupendra Singh, Rivka Shoulson, Anwesha Chatterjee, Amruta Ronghe, Nimee K Bhat, Daniel C Dim, Hari K Bhat

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
7.3field-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

78 citing papers in PubMed, 153 citations in OpenAlex.

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  12. Pharmaceuticals (Basel, Switzerland) · 2024
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18 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 3 institutions in 1 country.

Bhupendra SinghDepartment of Genetics, School of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA, Institute of Comparative Medicine, Columbia University, New York, NY 10032, USA and Division of Pharmacology and Toxicology, School of Pharmacy and School of Medicine, University of Missouri-Kansas City, Kansas City, MO 64108, USA.
Rivka ShoulsonInstitute of Comparative Medicine, Columbia University, New York, NY 10032, USA and.
Anwesha ChatterjeeDivision of Pharmacology and Toxicology, School of Pharmacy and.
Amruta RongheDivision of Pharmacology and Toxicology, School of Pharmacy and.
Nimee K BhatDivision of Pharmacology and Toxicology, School of Pharmacy and.
Daniel C DimSchool of Medicine, University of Missouri-Kansas City, Kansas City, MO 64108, USA.
Hari K BhatDivision of Pharmacology and Toxicology, School of Pharmacy and bhath@umkc.edu.
Columbia University · USUniversity of Alabama at Birmingham · USUniversity 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

The importance of estrogens in the etiology of breast cancer is widely recognized. Estrogen-induced oxidative stress has been implicated in this carcinogenic process. Resveratrol (Res), a natural antioxidant phytoestrogen has chemopreventive effects against a variety of illnesses including cancer. The objective of the present study was to characterize the mechanism(s) of Res-mediated protection against estrogen-induced breast carcinogenesis. Female August Copenhagen Irish rats were treated with 17β-estradiol (E2), Res and Res + E2 for 8 months. Cotreatment of rats with Res and E2 inhibited E2-mediated proliferative changes in mammary tissues and significantly increased tumor latency and reduced E2-induced breast tumor development. Resveratrol treatment alone or in combination with E2 significantly upregulated expression of nuclear factor erythroid 2-related factor 2 (NRF2) in mammary tissues. Expression of NRF2-regulated antioxidant genes NQO1, SOD3 and OGG1 that are involved in protection against oxidative DNA damage was increased in Res- and Res + E2-treated mammary tissues. Resveratrol also prevented E2-mediated inhibition of detoxification genes AOX1 and FMO1. Inhibition of E2-mediated alterations in NRF2 promoter methylation and expression of NRF2 targeting miR-93 after Res treatment indicated Res-mediated epigenetic regulation of NRF2 during E2-induced breast carcinogenesis. Resveratrol treatment also induced apoptosis and inhibited E2-mediated increase in DNA damage in mammary tissues. Increased apoptosis and decreased DNA damage, cell migration, colony and mammosphere formation in Res- and Res + E2-treated MCF-10A cells suggested a protective role of Res against E2-induced mammary carcinogenesis. Small-interfering RNA-mediated silencing of NRF2 inhibited Res-mediated preventive effects on the colony and mammosphere formation. Taken together, these results suggest that Res inhibits E2-induced breast carcinogenesis via induction of NRF2-mediated protective pathways.

Indexed as

AnimalsAnticarcinogenic AgentsAntioxidantsApoptosisBlotting, WesternCell MovementCell ProliferationCell Transformation, NeoplasticDNA MethylationEpigenesis, GeneticEstrogensFemaleHumansMammary Neoplasms, ExperimentalNF-E2-Related Factor 2Rats, Inbred ACIAnticarcinogenic AgentsAntioxidantsEstrogensNF-E2-Related Factor 2ResveratrolRNA, MessengerRNA, Small InterferingStilbenes

Identifiers

PMID24894866
PMCPMC4123650
OpenAlexW2141116428

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.