Evidence map›Paper›PMID 40196843›Full record

ArticleFrontiers in cell and developmental biology2025

Estrogen-induced FXR1 promotes endocrine resistance and bone metastasis in breast cancer via BCL2 and GPX4.

Yinzhong Shang, Tingfang Cao, Xin Ma, Le Huang, Mingming Wu, Junchao Xu, Jiarui Wang, Hao Wang, Sheng Wu, Vijay Pandey and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
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

15 authors.

Yinzhong Shang *Department of Oncology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, National Key Laboratory of Immune Response and Immunotherapy, University of Science and Technology of China, Hefei, China.
Tingfang Cao *Department of Oncology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, National Key Laboratory of Immune Response and Immunotherapy, University of Science and Technology of China, Hefei, China.
Xin MaTsinghua Shenzhen International Graduate School, Institute of Biopharmaceutical and Health Engineering, Shenzhen, China.
Le HuangDepartment of Oncology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, National Key Laboratory of Immune Response and Immunotherapy, University of Science and Technology of China, Hefei, China.
Mingming WuDepartment of Oncology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, National Key Laboratory of Immune Response and Immunotherapy, University of Science and Technology of China, Hefei, China.
Junchao XuDepartment of Oncology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, National Key Laboratory of Immune Response and Immunotherapy, University of Science and Technology of China, Hefei, China.
Jiarui WangDepartment of Oncology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, National Key Laboratory of Immune Response and Immunotherapy, University of Science and Technology of China, Hefei, China.
Hao WangDepartment of Pathology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Sheng WuDepartment of Oncology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, National Key Laboratory of Immune Response and Immunotherapy, University of Science and Technology of China, Hefei, China.
Vijay PandeyTsinghua Shenzhen International Graduate School, Institute of Biopharmaceutical and Health Engineering, Shenzhen, China.
Zhengsheng WuDepartment of Pathology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Weijie ZhangZhejiang Provincial Key Laboratory of Cancer Molecular Cell Biology, Life Sciences Institute, Zhejiang University, Hangzhou, China.
Peter E LobieShenzhen Bay Laboratory, Institute of Biomedical Health Technology and Engineering, Shenzhen, China.
Xinghua HanDepartment of Oncology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, National Key Laboratory of Immune Response and Immunotherapy, University of Science and Technology of China, Hefei, China.
Tao ZhuDepartment of Oncology, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, National Key Laboratory of Immune Response and Immunotherapy, University of Science and Technology of China, Hefei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Estrogen signaling dysregulation plays a critical role in the development of anti-estrogen resistance and bone metastasis of ER+ mammary carcinoma. Using quantitative proteomic screening, we identified FXR1 as an estrogen-regulated RNA-binding protein associated with anti-estrogen resistance. Mechanistically, estrogen and IGF1 facilitate FXR1 protein translation via the PI3K/AKT/mTOR/EIF4E pathway. FXR1 enhances cellular resistance to apoptosis and ferroptosis by facilitating the maturation of BCL2 pre-mRNA and stabilizing GPX4 mRNA, respectively. Anti-estrogen resistant cells exhibit elevated FXR1 expression, and FXR1 depletion restores their sensitivity to tamoxifen. Moreover, combining FXR1 depletion with a ferroptosis inducer induces synergistic lethal in anti-estrogen resistant cells. Finally, we provide proof-of-concept evidence supporting FXR1 antagonism as a potential treatment for bone metastases in ER+ breast cancer. Our findings highlight FXR1 as a promising therapeutic target to improve existing therapeutic regimes for ER+ breast cancer patients.

Indexed as

anti-estrogen resistanceapoptosisestrogenferroptosisFXR1

Identifiers

PMID40196843
PMCPMC11973456

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.