Evidence map›Paper›PMID 32492961›Full record

ArticleMolecules (Basel, Switzerland)2020

Quercetin Inhibits Lef1 and Resensitizes Docetaxel-Resistant Breast Cancer Cells.

Marta Prieto-Vila, Iwao Shimomura, Akiko Kogure, Wataru Usuba, Ryou-U Takahashi, Takahiro Ochiya, Yusuke Yamamoto

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
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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

7 authors at 3 institutions in 1 country.

Marta Prieto-VilaDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Iwao ShimomuraDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Akiko KogureDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Wataru UsubaDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Ryou-U TakahashiDepartment of Cellular and Molecular Biology, Hiroshima University, Hiroshima 734-8553, Japan.
Takahiro OchiyaDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Yusuke YamamotoDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Tokyo Medical University · JPHiroshima University · JPSt. Marianna University School of Medicine · JP

Funding

Japan Society for the Promotion of Science 17H04991Japan Society for the Promotion of Science 19K16761
6 · The paper itself

Abstract

Drug resistance is a major problem for breast cancer patients. Docetaxel is an anti-mitotic agent that serves as first line of treatment in metastatic breast cancer, however it is susceptible to cellular drug resistance. Drug-resistant cells are able to spread during treatment, leading to treatment failure and eventually metastasis, which remains the main cause for cancer-associated death. In previous studies, we used single-cell technologies and identified a set of genes that exhibit increased expression in drug-resistant cells, and they are mainly regulated by Lef1. Furthermore, upregulating Lef1 in parental cells caused them to become drug resistant. Therefore, we hypothesized that inhibiting Lef1 could resensitize cells to docetaxel. Here, we confirmed that Lef1 inhibition, especially on treatment with the small molecule quercetin, decreased the expression of Lef1 and resensitized cells to docetaxel. Our results demonstrate that Lef1 inhibition also downregulated ABCG2, Vim, and Cav1 expression and equally decreased Smad-dependent TGF-β signaling pathway activation. Likewise, these two molecules worked in a synergetic manner, greatly reducing the viability of drug-resistant cells. Prior studies in phase I clinical trials have already shown that quercetin can be safely administered to patients. Therefore, the use of quercetin as an adjuvant treatment in addition to docetaxel for the treatment of breast cancer may be a promising therapeutic approach.

Indexed as

Drug Resistance, NeoplasmATP Binding Cassette Transporter, Subfamily G, Member 2Breast NeoplasmsCaveolin 1Cell Line, TumorCell ProliferationCell SurvivalDocetaxelDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansInhibitory Concentration 50Lymphoid Enhancer-Binding Factor 1MCF-7 CellsNeoplasm MetastasisABCG2 protein, humanATP Binding Cassette Transporter, Subfamily G, Member 2CAV1 protein, humanCaveolin 1DocetaxelLEF1 protein, humanLymphoid Enhancer-Binding Factor 1Neoplasm ProteinsQuercetinRNA, Small InterferingTransforming Growth Factor betaVimentinVIM protein, humanbreast cancerdrug resistanceLef1quercetin

Identifiers

PMID32492961
PMCPMC7321307
OpenAlexW3030270073

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.