Long Noncoding RNA LINC00152 Facilitates the Leukemogenesis of Acute Myeloid Leukemia by Promoting CDK9 Through miR-193a.

The vital role of long noncoding RNAs (lncRNAs) on the acute myeloid leukemia (AML) has been increasingly recognized. This study aims to explore the unknown function of lncRNA LINC00152 in the leukemogenesis of AML. LINC00152 is determined to be upregulated in the AML samples, and the overexpression of LINC00152 is also authenticated in the advanced French-American-British (FAB) AML patients and closely correlated with the poor outcome of AML patients. The functional experiments state that knockdown of LINC00152 suppresses the proliferation, accelerates the apoptosis, and induces the cycle arrest of AML cells. The mechanical experiments state that LINC00152 and CDK9 were both targeted by miR-193a with the complementary binding sites at 3'-UTR. Moreover, in the rescue experiments, the enhanced LINC00152 expression could regain the suppression of tumor behavior induced by LINC00152 knockdown. In conclusion, this research reveals the important role of lncRNA LINC00152 in the AML leukemogenesis through targeting miR-193a/CDK9 axis. This finding could indicate the important pathogenesis of ncRNA and the vital roles of epigenetic regulation.