ArticleJournal of cellular and molecular medicine2025
Increasing RB1 Expression by Targeting EZH2 in Triple-Negative Breast Cancer.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Tumor heterogeneity in retinoblastoma: a literature review.Cancer metastasis reviews · 2025Review
- Integrating Single-Cell and Bulk RNA Sequencing Reveals the Malignant Phenotype of CBX4 in Prostate Cancer.Journal of Cancer · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Loss of RB1 function represents a defining characteristic of triple-negative breast cancer (TNBC) and is intricately associated with resistance to therapeutic interventions. In this study, we investigate the epigenetic mechanisms governing RB1 expression in TNBC. Employing a combination of bioinformatics analyses and experimental validations, we identified lysine histone methyltransferase EZH2 as a key upstream regulator of RB1 expression. EZH2 primarily mediates trimethylation of lysine 27 on histone H3 as the catalytic subunit of the Polycomb repressive complex 2 (PRC2) complex. Furthermore, our findings demonstrate that pharmacological inhibition of EZH2 leads to a significant upregulation of RB1 expression levels, mediated by enhanced enrichment of the activating histone marker H3K27ac at the RB1 enhancer region, as evidenced by ATAC-sequencing and ChIP-qPCR assays. These insights unveil a promising clinical avenue for combating RB1-mediated drug resistance in TNBC through the strategic integration of epigenetic-targeting agents.
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