ArticleOncogene2025
Super-enhancer-associated long noncoding RNA lnc-SPI1U mediates SPI1 feedback regulation by interacting with HNRNPH1 and HNRNPF.
Article in Oncogene, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
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Authors and funding
8 authors.
Funding
Abstract
Long noncoding RNAs (lncRNAs) have been extensively studied for their regulatory roles in gene expression; however, relatively little is known about those specifically associated with super-enhancers (SEs)-genomic elements crucial for maintaining cell identity and function. This study profiles acute promyelocytic leukemia (APL)-specific SE-associated lncRNAs (SE-lncRNAs) using H3K27ac ChIP-seq and RNA-seq data from TCGA and Beat AML cohorts, identifying 44 SE-lncRNAs potentially involved in APL pathogenesis. Among these, we characterized a novel SE-lncRNA, RP11-750H9.5, located upstream of the SPI1 gene encoding the hematopoietic transcription factor PU.1, and designated it as lnc-SPI1U. Functional assays demonstrated that lnc-SPI1U suppressed differentiation, apoptosis and ATRA-induced cell proliferation inhibition, contrasting with the established role of SPI1 in promoting differentiation. Mechanistically, lnc-SPI1U interacted with heterogeneous nuclear ribonucleoproteins HNRNPH1/F, destabilizing SPI1 mRNA. Furthermore, we found that the induction of lnc-SPI1U during myeloid differentiation was dependent on PU.1, which established a feedback loop to fine-tune SPI1 expression at the optimal level for myeloid differentiation. In APL, the PML/RARα fusion protein inhibited PU.1-dependent transactivation of lnc-SPI1U by hijacking the SE region that overlapped with lnc-SPI1U locus. Our study provides mechanistic insight into how SE-lncRNAs contribute to the precise regulation of transcription factor activity during myeloid differentiation.
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Registered trials
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