Evidence map›Paper›PMID 40492378›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Paracrine Orchestration of Tumor Microenvironment Remodeling Induced by GLO1 Potentiates Lymph Node Metastasis in Breast Cancer.

Jindong Xie, Wenjian Liu, Xinpei Deng, Huan Wang, Xueqi Ou, Xin An, Min-Yi Situ, Anli Yang, Chuan Peng, Rongfang He and 7 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

  1. Article
  2. C3Journal of translational medicine · 2026
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  8. A POSTNInternational journal of general medicine · 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

17 authors.

Jindong XieState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.ORCID 0000-0002-2482-7358
Wenjian LiuState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Xinpei DengState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Huan WangState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Xueqi OuState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Xin AnState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Min-Yi SituState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Anli YangState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Chuan PengState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Rongfang HeThe First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, China.
Yi XieState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Hailin TangState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Yuman ChenState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Jie-Ying LiangState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Ruonan ShaoState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Weikai XiaoDepartment of Breast Cancer, Guangdong Provincial People's Hospital and Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, China.
Shaoquan ZhengState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.

Funding

GuangDong Basic and Applied Basic Research Foundation 2023A1515111034National Natural Science Foundation of China 82003066National Natural Science Foundation of China 82403987Postdoctoral Fellowship Program of CPSF GZB20230903
6 · The paper itself

Abstract

Breast cancer is the most prevalent form of malignant tumor that frequently metastasizes to axillary lymph nodes (LNs). Nonetheless, the precise mechanisms underlying alterations in the tumor microenvironment (TME) in LN metastasis in breast cancer remain poorly understood. Single-cell RNA sequencing of 28 LN samples from 23 patients is performed, and a comprehensive landscape of the entire ecosystem is generated. Ten major cell types are identified, with the subclusters of each major cell type exhibiting diverse characteristics. Furthermore, multiple signatures are collected to evaluate the key components of the subclusters using multi-omics methodologies. This study finds that myCAFs may hasten LN metastasis, and observed a notable increase in APOE+ macrophages and a higher proportion of exhausted CD8+ T cells, contributing to the immunosuppressive TME. Moreover, cancer cells in metastatic lesions exhibited diverse expression patterns linked to proliferation, metastasis, oxidative phosphorylation, hypoxia, and interferon responses. Using multi-omics approaches and experimental validations, it determines that GLO1 can promote lymphatic angiogenesis, metastasis, and inhibit the proteasomal degradation of GSS, thereby maintaining intracellular glutathione (GSH) and reactive oxygen species (ROS) balance. Collectively, the study offers novel perspectives on the microenvironment remodeling of breast cancer LN metastases, suggesting that GLO1 may be a promising therapeutic target.

Indexed as

Breast NeoplasmsLymphatic MetastasisParacrine CommunicationTumor MicroenvironmentAnimalsFemaleHumansLymph NodesMicebreast cancerGLO1lymph node metastasesmulti‐omicstumor microenvironment

Identifiers

PMID40492378
PMCPMC12407353

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.