Evidence map›Paper›PMID 41543640›Full record

ArticleDiscover oncology2026

Integrated machine learning and bioinformatic analyses constructed a sulfur metabolism-related breast cancer risk model and identified heat-shock protein A9 as a potential therapeutic target for human breast cancer.

Yuan Yuan, Shuyao Zhang, Jialei Fu, Fei Zhou

Abstract read
In one paragraph

Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Yuan YuanPeking University Cancer Hospital, Beijing, China.
Shuyao ZhangXi'an Medical University, Xi'an, Shaanxi, China.
Jialei FuDepartment of Radiation Oncology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Fei ZhouDepartment of Radiation Oncology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China. feieryanjiu@qdu.edu.cn.

Funding

Affiliated Hospital of Qingdao University QDFY2023209
6 · The paper itself

Abstract

purposeOncogenesis and tumor progression have been linked to abnormal metabolism. We aimed to investigate the potential connection between sulfur metabolism-related genes and clinical features of patients with breast cancer.

methodsMachine learning algorithms were utilized to assess the risk index of sulfur metabolism-related genes in breast cancer. All patients were categorized into high- and low-risk clusters, based on their calculated average risk scores. Kaplan–Meier curves were used to evaluate the patient prognoses in different groups. Enrichment analysis was performed on the differentially expressed genes (DEGs) across these distinct clusters. The effect of the highest-risk gene, HSPA9, on the malignant behavior of tumor cells was appraised through siRNA transfection.

resultsA risk model with nine sulfur metabolism-related genes (ACOT2, ACOT4, CHPF, ELOVL2, HLCS, HSPA9, MICAL1, SPOCK2, and TCF7L2) was established, and low-risk groups exhibited better outcomes than high-risk groups. Various biological functions and pathways of the DEGs were observed between the different groups. The high-risk group exhibited a higher immune cell infiltration rate than the low-risk group. Inhibiting HSPA9 expression effectively reduced breast cancer cell proliferation and migration.

conclusionOur genetic risk model provides a novel pattern for prognostic evaluations and individualized therapeutic strategies for breast cancer. Given its association with breast cancer risk, HSPA9 represents an exceptionally promising therapeutic target.

Indexed as

Breast carcinomaGene signatureHeat-shock protein A9Prognostic modelSulfur metabolism

Identifiers

PMID41543640
PMCPMC12891319

What Socratic holds

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LicenceCC BY-NC-ND
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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.