Abstract
LncRNA CCDC26 is aberrantly expressed in myeloid leukemia (ML) and promotes myeloid leukemia progression, but the potential mechanism of CCDC26 in regulating ML progression is unclear. In this study, we observed that lncRNA CCDC26 was upregulated in both chronic and acute ML cell lines. LncRNA CCDC26 promoted the proliferation and invasion of K562 and HL-60 cells, which was determined by cell counting kit-8 test and Transwell invasion assay. Flow cytometry showed that lncRNA CCDC26 inhibited cell apoptosis. Bioinformatics and expression correlation analyses revealed that there was a potential interaction between CCDC26 and CUGBP Elav-like family member 2 (CELF2) protein, an RNA bind protein (RBP). Then the relationship between CCDC26 and the RBP CELF2 was identified by using RNA pull-down and RNA immunoprecipitation (RNA-IP) assays. Further analysis showed that overexpression of CCDC26 could noticeably upregulate circRNA_ANKIB1 expression via sponging CELF2. Subsequently, we found that overexpressed circRNA_ANKIB1 could significantly promote proline rich 11 (PRR11) protein expression by sponging miR-195a-5p. Moreover, PRR11 was also upregulated by CCDC26 and downregulated by CELF2. Mechanically, we uncovered that the miR-195a-5p inhibitor activated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways through upregulating PRR11 protein expression. Furthermore, the inhibitors of AKT, p65-NF-κB, or Bcl-2 could inhibit the effect of the miR-195a-5p inhibitor on ML cell behaviors. In conclusion, lncRNA CCDC26 could upregulate PRR11 protein expression by sponging miR-195a-5p, thereby activating the PI3K/AKT and NF-κB pathways to enhance ML cell proliferation and invasion and suppress cell apoptosis.