Long non-coding RNAs (lncRNAs) are important regulatory molecules that are implicated in cellular physiology and pathology. In this work, we dissect the functional role of the HOXB-AS3 lncRNA in patients with NPM1-mutated (NPM1mut) acute myeloid leukemia (AML). We show that HOXB-AS3 regulates the proliferative capacity of NPM1mut AML blasts in vitro and in vivo. HOXB-AS3 is shown to interact with the ErbB3-binding protein 1 (EBP1) and guide EBP1 to the ribosomal DNA locus. Via this mechanism, HOXB-AS3 regulates ribosomal RNA transcription and de novo protein synthesis. We propose that in the context of NPM1 mutations, HOXB-AS3 overexpression acts as a compensatory mechanism, which allows adequate protein production in leukemic blasts.
Bibliographical notePublisher Correction:
"The original version of this Article contained an error in the author affiliations.
Affiliation number 9 incorrectly read “Department of Molecular Medicine, University of Pavia, Pavia, USA”
This has now been corrected in both the PDF and HTML versions of the Article."
(Nat Commun 11:204 (2020). https://doi.org/10.1038/s41467-019-13969-7).
"The original version of this article omitted the following from the Acknowledgements: R.G. was supported by a Scholar in Clinical Research award from The Leukemia & Lymphoma Society."
This has now been corrected in both the PDF and HTML versions of the article.
(Nat Commun 11:3878 (2020). https://doi.org/10.1038/s41467-020-17746-9.