Evidence map›Paper›PMID 32661222›Full record

ArticleCell death & disease2020

Aspirin attenuates YAP and β-catenin expression by promoting β-TrCP to overcome docetaxel and vinorelbine resistance in triple-negative breast cancer.

Ji Ma, Zhenhai Fan, Qiulin Tang, Hongwei Xia, Tao Zhang, Feng Bi

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. GSK3β Regulates a Novel β-Catenin Degradation Pathway via the GID Complex in Wnt Signaling.Genes to cells : devoted to molecular & cellular mechanisms · 2025
    Article
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  7. E3 ubiquitin ligases in nasopharyngeal carcinoma and implications for therapies.Journal of molecular medicine (Berlin, Germany) · 2023
    Article
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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

6 authors at 2 institutions in 1 country.

Ji MaDepartment of Medical Oncology and Laboratory of Molecular Targeted Therapy in Oncology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, No. 37, Guoxue Lane, 610041, Chengdu, Sichuan, China.
Zhenhai FanKey Laboratory of Cell Engineering of Guizhou, The Affiliated Hospital of Zunyi Medical College, No. 149, Dalian Road, 573003, Zunyi, Guizhou, China.
Qiulin TangDepartment of Medical Oncology and Laboratory of Molecular Targeted Therapy in Oncology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, No. 37, Guoxue Lane, 610041, Chengdu, Sichuan, China.
Hongwei XiaDepartment of Medical Oncology and Laboratory of Molecular Targeted Therapy in Oncology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, No. 37, Guoxue Lane, 610041, Chengdu, Sichuan, China. hw.xia@scu.edu.cn.
Tao ZhangDepartment of Oncology, The General Hospital of Western Theater Command, No. 270, Tianhui Road, 610041, Chengdu, Sichuan Province, PR China. zhangtao269@126.com.
Feng BiDepartment of Medical Oncology and Laboratory of Molecular Targeted Therapy in Oncology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, No. 37, Guoxue Lane, 610041, Chengdu, Sichuan, China. bifeng@scu.edu.cn.
Sichuan University · CNAffiliated Hospital of Zunyi Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The use of aspirin has been associated with reduced breast cancer risk, but it is litter known if aspirin overcomes chemoresistance in triple-negative breast cancer (TNBC). Herein, we demonstrated that changes in the expression of Yes-associated protein (YAP) and β-catenin might be a promising predictive biomarker for neoadjuvant chemotherapy sensitivity in TNBC patients. Inhibition of YAP or β-catenin enhanced the cytotoxicity of the anti-microtubule agents docetaxel and vinorelbine against drug-resistant TNBC cells as well as the sensitivity of these cells to the agents in vitro and in vivo. Interestingly, aspirin not only significantly inhibited the growth of TNBC cells, but also attenuated YAP and β-catenin expression by upregulating the E3 ubiquitin ligase β-TrCP to abolished docetaxel and vinorelbine resistance. The combination of aspirin and docetaxel or vinorelbine remarkably inhibited the growth of drug-resistant TNBC cells in vitro and in vivo. Moreover, TNBC patients with high YAP and/or β-catenin expression had a higher risk of relapse or mortality than patients with low YAP and/or β-catenin expression. Collectively, our study discovered a novel role of aspirin based on its anticancer effect, and put forward some possible mechanisms of chemoresistance in TNBC. The combined use of aspirin and anti-microtubule drugs presented several promising therapeutic approaches for TNBC treatment.

Indexed as

AnimalsAspirinbeta CateninCell Cycle ProteinsDisease Models, AnimalDrug Resistance, NeoplasmFemaleHumansMiceMice, NudeTranscription FactorsTriple Negative Breast NeoplasmsAspirinbeta CateninCell Cycle ProteinsTranscription FactorsYY1AP1 protein, human

Identifiers

PMID32661222
PMCPMC7359325
OpenAlexW3042171914

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.