ArticleCell death & disease2025
Super enhancer lncRNA RP11-54O7.17 regulates the proliferation and metastasis of triple-negative breast cancer by targeting lysosomal degradation of S100A4.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- METTL14-Mediated m6A Modification of NEAT1_2 Releases YBX1 From Paraspeckles to Exacerbate Periodontitis.Journal of clinical periodontology · 2026Article
- Super-enhancer-driven ITGB2-AS1 promotes ovarian cancer progression by binding to IQGAP1.Translational oncology · 2026Article
- HDHD5 promotes triple-negative breast cancer growth and drives EMT-associated phenotypes via regulating S100A4.Journal of cancer research and clinical oncology · 2026Article
- Identification of MTFR1 as a Novel Prognostic Biomarker and Putative Oncogene for Breast Cancer: A Multi-Omics Analysis and in Vitro Experimental Validation.IET systems biologyArticle
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Authors and funding
9 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) is characterized by its high aggressiveness and treatment resistance, with limited therapeutic options and especially a lack of effective targeted therapeutic strategies. This study focuses on the role and regulatory mechanisms of super enhancer long non-coding RNA (SE-lncRNA) in TNBC. Through in-depth analysis of TCGA database, we revealed the specific expression pattern of SE-lncRNA in TNBC, and found that downregulation of RP11-54O7.17 was significantly correlated with poor prognosis of TNBC patients, which was experimentally verified. Both in vitro and in vivo results confirmed that RP11-54O7.17 overexpression effectively suppressed the proliferation and metastasis of TNBC. Further exploration showed that RP11-54O7.17 directly interacted with the S100A4 protein through its conserved L2b-type repeat structural fragment, promoted S100A4 binding to HSP70, targeting S100A4 degradation via the autophagy-lysosome pathway, which in turn blocked the activation of S100A4-STAT3 signaling axis. Moreover, RP11-54O7.17 delivered via liposome demonstrated significant anti-TNBC efficacy in an in vivo model without observing significant systemic toxicity. This study elucidates the regulatory role and molecular mechanism of RP11-54O7.17 in TNBC, which provides a strong scientific basis and potential therapeutic targets for the development of novel SE-lncRNA-based therapeutic strategies.
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