The lncRNA CASC15 regulates SOX4 expression in RUNX1-rearranged acute leukemia

Thilini R. Fernando, Jorge R. Contreras, Matteo Zampini, Norma I. Rodriguez-Malave, Michael O. Alberti, Jaime Anguiano, Tiffany M. Tran, Jayanth K. Palanichamy, Jasmine Gajeton, Nolan M. Ung, Cody J. Aros, Ella V. Waters, David Casero, Giuseppe Basso, Martina Pigazzi, Dinesh S. Rao

Research output: Contribution to journalArticlepeer-review

89 Scopus citations


Background: Long non-coding RNAs (lncRNAs) play a variety of cellular roles, including regulation of transcription and translation, leading to alterations in gene expression. Some lncRNAs modulate the expression of chromosomally adjacent genes. Here, we assess the roles of the lncRNA CASC15 in regulation of a chromosomally nearby gene, SOX4, and its function in RUNX1/AML translocated leukemia. Results: CASC15 is a conserved lncRNA that was upregulated in pediatric B-acute lymphoblastic leukemia (B-ALL) with t (12; 21) as well as pediatric acute myeloid leukemia (AML) with t (8; 21), both of which are associated with relatively better prognosis. Enforced expression of CASC15 led to a myeloid bias in development, and overall, decreased engraftment and colony formation. At the cellular level, CASC15 regulated cellular survival, proliferation, and the expression of its chromosomally adjacent gene, SOX4. Differentially regulated genes following CASC15 knockdown were enriched for predicted transcriptional targets of the Yin and Yang-1 (YY1) transcription factor. Interestingly, we found that CASC15 enhances YY1-mediated regulation of the SOX4 promoter. Conclusions: Our findings represent the first characterization of this CASC15 in RUNX1-translocated leukemia, and point towards a mechanistic basis for its action.

Original languageEnglish
Article number126
JournalMolecular Cancer
Issue number1
StatePublished - Jul 19 2017


  • B-all
  • CASC15
  • ETV6-RUNX1
  • Non-coding RNA
  • SOX4


Dive into the research topics of 'The lncRNA CASC15 regulates SOX4 expression in RUNX1-rearranged acute leukemia'. Together they form a unique fingerprint.

Cite this