Evidence map›Paper›PMID 40890129›Full record

ArticleCell death & disease2025

YY1-induced USP43 drives ferroptosis suppression by FASN stabilization and subsequent activation of SLC7A11 in ovarian cancer.

Tianyi Zhao, Xiaojun Chen, Jiangchun Wu, Siyu Chen, Yu Gan, Chaohua Liu, Xinyu Ha, Yangjun Wu, Xiang Zhou, Yong Wu and 1 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

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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

11 authors.

Tianyi Zhao *Department of Gynecologic Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Xiaojun Chen *Department of Gynecologic Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Jiangchun Wu *Department of Gynecologic Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Siyu Chen *Department of Gynecologic Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Yu GanDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Chaohua LiuDepartment of Gynecologic Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Xinyu HaDepartment of Gynecologic Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Yangjun WuDepartment of Gynecologic Oncology, Fudan University Shanghai Cancer Center, Shanghai, China. wuyangjun1014@163.com.ORCID http://orcid.org/0000-0002-3055-208X
Xiang ZhouDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, China. xiangzhou@fudan.edu.cn.ORCID http://orcid.org/0000-0002-1172-7948
Yong WuDepartment of Gynecologic Oncology, Fudan University Shanghai Cancer Center, Shanghai, China. docwuyong@outlook.com.
Xiaohua WuDepartment of Gynecologic Oncology, Fudan University Shanghai Cancer Center, Shanghai, China. wu.xh@fudan.edu.cn.ORCID http://orcid.org/0000-0002-7664-8327

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82002747National Natural Science Foundation of China (National Science Foundation of China) 82272898
6 · The paper itself

Abstract

The ubiquitin-specific protease (USP) family is a major member of the deubiquitinating enzyme family that plays important and diverse roles in multiple tumors. The roles and mechanisms of action of USP family members in ovarian cancer are not well understood. This study aimed to screen all the USP family members and explored the specific function of USP43 in ovarian cancer. The expression levels of USP family members in ovarian cancer were screened using bioinformatics analysis, and the specific function of USP43 was explored through in vitro and in vivo experiments. Functional assays, including cell viability, ferroptosis, and tumor xenograft models, were employed. In short, USP43 drives the ferroptosis suppression by activating the expression of SLC7A11 through FASN-HIF1α pathway. USP43 is an important prognostic factor for ovarian cancer, with its overexpression promoting ovarian cancer progression and its knockdown inhibiting it. Mechanistically, USP43, which is transcriptionally activated by YY1, stabilizes FASN through deubiquitination, and FASN activates SLC7A11 expression by stabilizing HIF1α. Furthermore, the combination of cisplatin and the SLC7A11 inhibitor HG106 significantly inhibits the growth of ovarian tumors. Thus, targeting the USP43-FASN-HIF1α-SLC7A11 axis can inhibit ferroptosis and promote platinum sensitivity in ovarian cancer.

Indexed as

Amino Acid Transport System y+Fatty Acid Synthase, Type IFerroptosisOvarian NeoplasmsUbiquitin-Specific ProteasesYY1 Transcription FactorAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitMiceMice, Inbred BALB CMice, NudeAmino Acid Transport System y+FASN protein, humanFatty Acid Synthase, Type IHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitSLC7A11 protein, humanUbiquitin-Specific ProteasesYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID40890129
PMCPMC12402158

What Socratic holds

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LicenceCC BY
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Registered trials

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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 Socratic graph.