Evidence map›Paper›PMID 35182054›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022

YAP Dictates Mitochondrial Redox Homeostasis to Facilitate Obesity-Associated Breast Cancer Progression.

Jia-Zih Dai, Yen-Ju Wang, Cheng-Hsun Chen, I-Lin Tsai, Yi-Chun Chao, Cheng-Wei Lin

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. 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
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

16 citing papers in PubMed, 24 citations in OpenAlex.

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  14. Targeting Breast Cancer Stem Cells.International journal of biological sciences · 2023
    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

6 authors at 2 institutions in 1 country.

Jia-Zih DaiDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, 110, Taiwan.
Yen-Ju WangDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, 110, Taiwan.
Cheng-Hsun ChenDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, 110, Taiwan.ORCID 0000-0003-4622-2680
I-Lin TsaiDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, 110, Taiwan.
Yi-Chun ChaoDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, 110, Taiwan.
Cheng-Wei LinDepartment of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, 110, Taiwan.
Taipei Medical University · TWKaohsiung Medical University · TW

Funding

Chi Mei Medical Center 109CM-TMU-03Chi Mei Medical Center 110CM-TMU-01Ministry of Science and Technology, Taiwan MOST106-2320-B-038-040Ministry of Science and Technology, Taiwan MOST107-2320-B-038-052-MY3Ministry of Science and Technology, Taiwan MOST110-2320-B-038-021
6 · The paper itself

Abstract

Dysregulation of hormones is considered a risk factor for obesity-mediated breast tumorigenesis; however, obesity is associated with poor outcomes among women diagnosed with triple-negative breast cancer (TNBC), which is a hormone-independent breast cancer subtype. Thus, identifying the driving force behind the obesity-breast cancer relationship is an urgent need. Here it is identified that diet-induced obesity (DIO) facilitates tumorigenesis of TNBC cells. Mechanistically, DIO induces a metabolic addiction to fatty acid oxidation (FAO), accompanied by coordinated activation of Yes-associated protein (YAP) signaling. Specifically, YAP governs mitochondrial redox homeostasis via transcriptional regulation of antioxidant-related enzymes, which renders tumor cells capable of extenuating FAO-elicited mitochondrial oxidative stress. Moreover, adipocytes-derived fatty acids are identified to be responsible for enhancing the FAO-YAP axis and antioxidative capacity, and higher expression of an obesity signature in breast cancer patients is positively correlated with YAP signaling and antioxidant genes. The findings uncover the crucial role of YAP in dictating mitochondrial redox homeostasis for obesity-mediated metabolic adaptation and breast tumor progression.

Indexed as

Triple Negative Breast NeoplasmsAntioxidantsCarcinogenesisFemaleHomeostasisHumansObesityOxidation-ReductionTranscription FactorsAntioxidantsTranscription Factorsbreast cancerfatty acid oxidationobesityoxidative phosphorylationYAP

Identifiers

PMID35182054
PMCPMC9035999
OpenAlexW4213177165

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.