ORIGINAL RESEARCH article
Front. Oncol.
Sec. Cancer Molecular Targets and Therapeutics
This article is part of the Research TopicInnovative Strategies for the Discovery of New Therapeutic Targets in Cancer TreatmentView all 9 articles
Role of SUV39H2 in Shaping the Malignant Phenotype of Triple-Negative Breast Cancer
Provisionally accepted
- 1Wuhan University of Science and Technology, Wuhan, China
- 2Jianghan University, Wuhan, China
- 3Yueyang Vocational Technical College, yueyang, China
- 4Yueyang Hospital Affiliated to Hunan Normal University Department of Anesthesiology, yueyang, China
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Abstract Background SUV39H2, a histone methyltransferase involved in H3K9 trimethylation and transcriptional silencing, has been implicated in cancer progression. However, its expression patterns, clinical relevance, and functional roles in various tumor types remain to be fully elucidated. Methods SUV39H2 expression in multiple cancers and paired adjacent normal tissues was analyzed using the TCGA-GTEX database and Xiantao online tools. Prognostic significance was assessed by survival analysis. KEGG and GO enrichment analyses were conducted to explore potential functional roles. Immune infiltration correlations were evaluated based on TCGA data. Single-cell RNA sequencing from GSE176078 was analyzed for validation of expression patterns. Immunohistochemistry (IHC) was performed on five pairs of TNBC patient samples to confirm SUV39H2 expression. Western blotting (WB) was conducted to verify SUV39H2 knockdown efficiency in MDA-MB-231 and Hs-578T TNBC cells. Functional assays, including Transwell migration, colony formation, sphere formation, and subcutaneous xenograft tumorigenicity assays, were performed to evaluate the effects of SUV39H2 knockdown on TNBC cell growth and metastatic potential. Results SUV39H2 was significantly overexpressed in multiple cancers, with consistently elevated levels in paired tumor-adjacent tissues. In TNBC, SUV39H2 expression was markedly upregulated across all clinical and TNM stages compared with normal tissues and other BRCA subtypes. Immunohistochemistry confirmed SUV39H2 overexpression in TNBC patient samples, and WB demonstrated successful knockdown in MDA-MB-231 and Hs-578T cells. Functional assays revealed that SUV39H2 knockdown significantly inhibited proliferation, migration, stemness, and in vivo tumorigenicity in TNBC cells. Conclusions SUV39H2 is consistently upregulated in triple-negative breast cancer and is associated with malignant features including enhanced proliferation, migration, stemness, and in vivo tumorigenicity. Functional and clinical evidence highlights SUV39H2 as a potential diagnostic biomarker and therapeutic target in TNBC, although its clinical utility requires further validation.
Keywords: SUV39H2, TNBC, Diagnostic biomarker, BRCA subtypes, TCGA
Received: 04 Aug 2025; Accepted: 07 Nov 2025.
Copyright: © 2025 Deng, Wang, Hu, Chen, Lu, Jiang and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Yang Deng, dengyang@wust.edu.cn
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