ArticleCellular oncology (Dordrecht, Netherlands)2023
H3K27 acetylation activated long noncoding RNA RP11-162G10.5 promotes breast cancer progression via the YBX1/GLO1 axis.
Article in Cellular oncology (Dordrecht, Netherlands), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- A narrative review of epigenetic marker in H3K27ac and its emerging potential as a therapeutic target in cancer.Epigenomics · 2025Review
- YBX1: an RNA/DNA-binding protein that affects disease progression.Frontiers in oncology · 2025Review
- Long Non-coding RNA 02298 Promotes the Malignancy of HCC by Targeting the miR-28-5p/CCDC6 Pathway.Biochemical genetics · 2024Article
- CircMAN1A2_009 facilitates YBX1 nuclear localization to induce GLO1 activation for cervical adenocarcinoma cell growth.Cancer science · 2024Article
- Article
- Y-Box Binding Protein 1: Unraveling the Multifaceted Role in Cancer Development and Therapeutic Potential.International journal of molecular sciences · 2024Review
- Article
- Emerging roles of interactions between ncRNAs and other epigenetic modifications in breast cancer.Frontiers in oncology · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeLong noncoding RNAs (lncRNAs) orchestrate critical roles in human tumorigenesis. However, the regulatory mechanism of lncRNAs in tissue-specific expressions in breast cancer (BC) remains poorly understood. This study aims to investigate lncRNA role and mechanisms in BC.
methodsRNA sequencing was used to explore differentially expressed lncRNAs in BC and adjacent tissues. H3K27 acetylation (H3K27ac) chromatin immune-precipitation sequencing (ChIP-seq) data of BC cells from the GEO dataset (GSE85158) was retrieved to identify the H3K27ac activated lncRNAs that were involved in tumorigenesis. RP11-162G10.5 was selected as the target lncRNA for further functional and mechanism study.
resultsIn this study, we identified a novel lncRNA RP11-162G10.5, whose overexpression was specifically driven by H3K27ac in luminal breast cancer. And increased RP11-162G10.5 in BC is correlated with poor patient outcomes. RP11-162G10.5 promotes tumor cell proliferation in vitro and in vivo. Mechanistically, RP11-162G10.5 recruits transcriptional factor YBX1 to the GLO1 promoter, consequently activating GLO1 transcription to modulate the progression of BC.
conclusionsOur findings suggest that the histone modification-activated lncRNA contributes to the oncogenesis of BC. Also, our data reveal a role for RP11-162G10.5 in BC tumorigenesis and may supply a strategy for targeting the RP11-162G10.5 as a potential biomarker and a therapeutic target for breast cancer patients.
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