Long non-coding RNA (lncRNA) LINC00899 is one kind cytoplasmic lncRNA, however, there is rarely little information about its function in physiological process. Here, we demonstrated that lncRNA LINC00899 was upregulated in acute myeloid leukaemia (AML) cells and was quite correlated with poor prognosis of AML patients. High expression of LINC00899 in AML cells could promote cell proliferation and inhibit cell apoptosis, and facilitate the progression of AML consequently both in vitro and in vivo. Besides, LINC00899 acted as a molecular sponge of miR-744-3p. Furthermore, we characterized YY1 as the direct target of miR-744-3p, and LINC00899/miR-744-3p interaction modulated YY1 expression in AML cells. Finally, we verified LINC00899 modulated AML cell proliferation and apoptosis via regulating YY1. Our study revealed novel mechanism about how did lncRNA LINC00899 execute function in AML and thus provided potential therapeutic interventions for AML. SIGNIFICANCE OF THE STUDY: LncRNA LINC00899 is upregulated in AML cells and is correlated with poor prognosis of AML patients. LncRNA LINC00899 mediates cell proliferation and apoptosis of acute myeloid leukaemia cells. Knockdown of LINC00899 inhibited the growth of xenograft glioma tumour in vivo. LINC00899 acts as a molecular sponge of miR-744-3p. YY1 is the downstream target of LINC00899/miR-744-3p signalling.
Keywords: LINC00899; LncRNA; YY1; acute myeloid leukaemia; miR-744-3p.
© 2020 John Wiley & Sons Ltd.