Evidence map›Paper›PMID 28191286›Full record

ArticleGenes & cancer2016

The regulation of tumor suppressor protein, p53, and estrogen receptor (ERα) by resveratrol in breast cancer cells.

Julieta Saluzzo, Kelly M Hallman, Katie Aleck, Brigitte Dwyer, Meghan Quigley, Viktoria Mladenovik, Amy E Siebert, Sumi Dinda

Open access · diamondAbstract read
In one paragraph

Article in Genes & cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Myricetin Apoptotic Effects on T47D Breast Cancer Cells is a P53-Independent Approach.Asian Pacific journal of cancer prevention : APJCP · 2020
    Article
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  6. Review
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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

8 authors at 1 institution in 1 country.

Julieta SaluzzoSchool of Health Sciences, Oakland University, Rochester, MI, USA; Prevention Research Center, Oakland University, Rochester, MI, USA.
Kelly M HallmanSchool of Health Sciences, Oakland University, Rochester, MI, USA; Prevention Research Center, Oakland University, Rochester, MI, USA.
Katie AleckSchool of Health Sciences, Oakland University, Rochester, MI, USA; Prevention Research Center, Oakland University, Rochester, MI, USA.
Brigitte DwyerSchool of Health Sciences, Oakland University, Rochester, MI, USA; Prevention Research Center, Oakland University, Rochester, MI, USA.
Meghan QuigleySchool of Health Sciences, Oakland University, Rochester, MI, USA; Prevention Research Center, Oakland University, Rochester, MI, USA.
Viktoria MladenovikSchool of Health Sciences, Oakland University, Rochester, MI, USA; Prevention Research Center, Oakland University, Rochester, MI, USA.
Amy E SiebertSchool of Health Sciences, Oakland University, Rochester, MI, USA; Prevention Research Center, Oakland University, Rochester, MI, USA.
Sumi DindaSchool of Health Sciences, Oakland University, Rochester, MI, USA; Prevention Research Center, Oakland University, Rochester, MI, USA.
Oakland University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Resveratrol (RES) is a natural antioxidant found abundantly in grapes, peanuts, and berries, and is known to possess anti-tumorigenic properties. However, there is a noticeable lack of studies on the mechanistic effects of Resveratrol on tumor suppressors. Previous studies from our laboratory have shown the tumor suppressor protein p53 and estrogen receptor-alpha (ERα) to be possible molecular targets for RES. In this study, the anti-estrogenic effects of RES were analyzed on the expression of ERα and p53. The breast cancer cells grown in stripped serum were treated with 60 μM RES, as the optimum concentration based on data obtained from a concentration study using 1-100 μM RES. Our studies indicate that RES caused a decrease in the levels of protein expression of p53 and ERα as compared to the control. Increasing concentrations of RES caused a four-fold decrease in cell number in comparison to estradiol. RES, in conjunction with ICI 182,780 (ICI), caused a down-regulation of both p53 and ERα as compared to the control. These observed effects on cell proliferation and regulation of both p53 and ERα by RES may lead to further understanding of the relationship between tumor suppressor proteins and steroid receptors in breast cancer cells.

Indexed as

antiestrogensBreast cancerestrogenp53tumor suppressors

Identifiers

PMID28191286
PMCPMC5302041
OpenAlexW2981962998

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.