LncRNA Promotes the Progression of B-cell Precursor Acute Lymphoblastic Leukemia by Targeting the /CREB Axis.

The imbalance between the proliferation and apoptosis of B-cell precursors is an important contributor to the pathogenesis of B-cell precursor acute lymphoblastic leukemia (BCP-ALL), while its specific regulatory mechanism remains perplexing. This study aimed to expound the underlying mechanism of the proliferation and apoptosis of BCP-ALL cells from the perspective of non-coding RNA. In this study, long non-coding RNA colorectal neoplasia differentially expressed (LncRNA ) was upregulated in the bone marrow of BCP-ALL patients and BCP-ALL cell lines (NALM-6 and RS4;11). Functionally, LncRNA knockdown restrained cell proliferation and boosted cell apoptosis in NALM-6 and RS4;11 cells. The subsequent investigation confirmed that LncRNA bound to and negatively regulated expression. The overexpression of suppressed cell proliferation and boosted cell apoptosis in NALM-6 and RS4;11 cells. Further experiments revealed that downregulated cyclic AMP response element-binding protein (CREB) expression by targeting its mRNA directly. overexpression reversed the effect of mimic on cell proliferation and apoptosis in NALM-6 and RS4;11 cells. Finally, experiments showed that LncRNA knockdown prolonged the survival of mice xenotransplanted with NALM-6 cells. In conclusion, LncRNA upregulated CREB expression by suppressing , thus promoting cell proliferation and reducing cell apoptosis in BCP-ALL.