Evidence map›Paper›PMID 39833180›Full record

ArticleCell death & disease2025

Targeting estrogen-regulated system x

Jiawei Cao, Tong Zhou, Tao Wu, Rixu Lin, Ju Huang, Dejin Shi, Jiawei Yu, Yinrui Ren, Changrui Qian, Licai He and 4 more

Abstract read
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 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

  1. Estrogen Receptor Beta Isoforms Interplay Integrates Nuclear and Extra-Nuclear Signaling to Modulate Human Granulosa Cell Growth.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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

14 authors.

Jiawei Cao *Wenzhou Key Laboratory of Cancer Pathogenesis and Translation, Key Laboratory of Laboratory Medicine, School of Laboratory Medicine and Life Sciences, Ministry of Education, Wenzhou Medical University, 325035, Wenzhou, China. jiaweicao@wmu.edu.cn.ORCID 0000-0001-6268-5912
Tong Zhou *Wenzhou Key Laboratory of Cancer Pathogenesis and Translation, Key Laboratory of Laboratory Medicine, School of Laboratory Medicine and Life Sciences, Ministry of Education, Wenzhou Medical University, 325035, Wenzhou, China.
Tao WuWenzhou Key Laboratory of Cancer Pathogenesis and Translation, Key Laboratory of Laboratory Medicine, School of Laboratory Medicine and Life Sciences, Ministry of Education, Wenzhou Medical University, 325035, Wenzhou, China.
Rixu LinDepartment of Pathology, The First Affiliated Hospital of Wenzhou Medical University, 325035, Wenzhou, China.
Ju HuangWenzhou Key Laboratory of Cancer Pathogenesis and Translation, Key Laboratory of Laboratory Medicine, School of Laboratory Medicine and Life Sciences, Ministry of Education, Wenzhou Medical University, 325035, Wenzhou, China.
Dejin ShiWenzhou Key Laboratory of Cancer Pathogenesis and Translation, Key Laboratory of Laboratory Medicine, School of Laboratory Medicine and Life Sciences, Ministry of Education, Wenzhou Medical University, 325035, Wenzhou, China.
Jiawei YuWenzhou Key Laboratory of Cancer Pathogenesis and Translation, Key Laboratory of Laboratory Medicine, School of Laboratory Medicine and Life Sciences, Ministry of Education, Wenzhou Medical University, 325035, Wenzhou, China.
Yinrui RenWenzhou Key Laboratory of Cancer Pathogenesis and Translation, Key Laboratory of Laboratory Medicine, School of Laboratory Medicine and Life Sciences, Ministry of Education, Wenzhou Medical University, 325035, Wenzhou, China.
Changrui QianSchool of Basic Medical Sciences, Wenzhou Medical University, 325035, Wenzhou, China.
Licai HeWenzhou Key Laboratory of Cancer Pathogenesis and Translation, Key Laboratory of Laboratory Medicine, School of Laboratory Medicine and Life Sciences, Ministry of Education, Wenzhou Medical University, 325035, Wenzhou, China.
Guang WuWenzhou Key Laboratory of Cancer Pathogenesis and Translation, Key Laboratory of Laboratory Medicine, School of Laboratory Medicine and Life Sciences, Ministry of Education, Wenzhou Medical University, 325035, Wenzhou, China.
Zhixiong DongWenzhou Key Laboratory of Cancer Pathogenesis and Translation, Key Laboratory of Laboratory Medicine, School of Laboratory Medicine and Life Sciences, Ministry of Education, Wenzhou Medical University, 325035, Wenzhou, China.ORCID 0000-0001-7281-671X
Shaofei YuanDepartment of Medical Oncology, Rui'an People's Hospital, The Third Affiliated Hospital of Wenzhou Medical University, 325200, Wenzhou, China. ysf1004@wmu.edu.cn.
Haihua GuWenzhou Key Laboratory of Cancer Pathogenesis and Translation, Key Laboratory of Laboratory Medicine, School of Laboratory Medicine and Life Sciences, Ministry of Education, Wenzhou Medical University, 325035, Wenzhou, China. haihuagu@wmu.edu.cn.ORCID 0000-0003-2154-9900

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82272702National Natural Science Foundation of China (National Science Foundation of China) 82302925Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LQ23H160012Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LTGY23H080005Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LZ23H160001
6 · The paper itself

Abstract

Estrogen receptor positive (ER+) breast cancer accounts for approximately 70% of cases. Endocrine therapies targeting estrogen are the first line therapies for ER+ breast cancer. However, resistance to these therapies occurs in about half of patients, leading to decreased survival rates. Inducing ferroptosis is a promising therapeutic strategy for cancer treatment for refractory and malignant cancers including triple-negative breast cancer. Nevertheless, ER+ breast cancer is relatively resistant to ferroptosis inducers. Here, we uncovered that ERα suppressed ferroptosis in ER+ breast cancer. Silencing ERα triggered ferroptosis, which was attenuated by ferroptosis inhibitor Ferrostatin-1, and was enhanced by ferroptosis inducer Erastin. Mechanistically, ERα transcriptionally upregulated the expression of SLC7A11 and SLC3A2, two subunits of the system x

Indexed as

Amino Acid Transport System y+Breast NeoplasmsEstrogen Receptor alphaEstrogensFerroptosisAnimalsCell Line, TumorDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMiceMice, Inbred BALB CMice, NudePiperazinesAmino Acid Transport System y+erastinEstrogen Receptor alphaEstrogensPiperazinesReceptors, EstrogenSLC7A11 protein, humanTamoxifen

Identifiers

PMID39833180
PMCPMC11756422

What OpenQuestion holds

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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 OpenQuestion graph.