Evidence map›Paper›PMID 34737887›Full record

ArticleFuture science OA2021

Combination of quercetin and 2-methoxyestradiol inhibits epithelial-mesenchymal transition in PC-3 cell line via Wnt signaling pathway.

Neeti Sharma, Piyush W Raut, Meghna M Baruah, Akshay Sharma

Open access · goldAbstract read
In one paragraph

Article in Future science OA, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. 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

4 authors at 2 institutions in 1 country.

Neeti SharmaSchool of Engineering, Ajeenkya DY Patil University, Charholi Budruk, Pune, 412105, India.ORCID https://orcid.org/0000-0002-4457-5717
Piyush W RautSymbiosis School of Biological Sciences, Symbiosis International (Deemed University), Gram - Lavale; Taluka - Mulshi, Pune, India.ORCID https://orcid.org/0000-0002-8292-6848
Meghna M BaruahSymbiosis School of Biological Sciences, Symbiosis International (Deemed University), Gram - Lavale; Taluka - Mulshi, Pune, India.ORCID https://orcid.org/0000-0003-4748-6151
Akshay SharmaSymbiosis School of Biological Sciences, Symbiosis International (Deemed University), Gram - Lavale; Taluka - Mulshi, Pune, India.
Symbiosis International University · IND.Y. Patil University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimWe have previously reported that quercetin (Qu) regulates epithelial-mesenchymal transition (EMT) by modulating Wnt signaling components. In this study, we investigated the synergistic effect of Qu and 2-methoxyestradiol (2-ME) and the role of Wnt signaling components in regulating EMT in PC-3 cells. MATERIALS &

methodsEMT was induced by treating PC-3 cells with TGF-β, followed by evaluation of expression of EMT markers and Wnt signaling proteins in naive, induced and after exposing induced cells to Qu and 2-ME at both gene and protein level by real-time PCR (RT-PCR) and western blot, respectively.

resultsQu and 2-ME synergistically downregulated mesenchymal markers with simultaneous upregulation of epithelial markers. Wnt signaling proteins expression was also downregulated by Qu and 2-ME in TGF-β-induced EMT in PC-3 cells.

conclusionThus, combination therapy of Qu and 2-ME could be a new promising therapeutic approach for the treatment of prostate cancer.

Indexed as

2-methoxyestradiolEMTmetastasisprostate cancerquercetinWnt signaling

Identifiers

PMID34737887
PMCPMC8558868
OpenAlexW3201908861

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.