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Background  Long non-coding RNAs (lncRNAs) are recognized as pivotal players during developmental ontogenesis and pathogenesis of cancer. The intronic microRNA (miRNA) clusters  miR-99a ~ 125b-2  and  miR-100 ~ 125b-1  promote progression of acute megakaryoblastic leukemia (AMKL), an aggressive form of hematologic cancers. The function of the lncRNA hostgenes  MIR99AHG  (alias  MONC ) and  MIR100HG  within this ncRNA ensemble remained elusive.    Results  Here we report that lncRNAs  MONC  and  MIR100HG  are highly expressed in AMKL blasts. The transcripts were mainly localized in the nucleus and their expression correlated with the corresponding miRNA clusters. Knockdown of  MONC  or  MIR100HG  impeded leukemic growth of AMKL cell lines and primary patient samples. The development of a lentiviral lncRNA vector to ectopically express lncRNAs without perturbing their secondary structure due to improper termination of the viral transcript, allowed us to study the function of  MONC  independent of the miRNAs in cord blood hematopoietic stem and progenitor cells (HSPCs). We could show that  MONC  interfered with hematopoietic lineage decisions and enhanced the proliferation of immature erythroid progenitor cells.    Conclusions  Our study reveals an unprecedented function of lncRNAs  MONC  and  MIR100HG  as regulators of hematopoiesis and oncogenes in the development of myeloid leukemia.

LincRNAs MONC and MIR100HG act as oncogenes in acute megakaryoblastic leukemia