Long non-coding RNA LINC00641 promotes cell growth and migration through modulating miR-378a/ZBTB20 axis in acute myeloid leukemia

摘要

OBJECTIVE: Many researchers have revealed that long noncoding RNAs (lncRNAs) acted as modulators in tumor biology. LncRNA LINC00641 (LINC00641), a newly discovered tumor-related lncRNA, has been reported to act as a modulator in several tumors. Hence, our study aimed to examine the expression and function of LINC00641 in acute myeloid leukemia (AML). PATIENTS AND METHODS: The expression pattern of LINC00641 in AML specimens and cell lines was explored using a gene expression profiling interactive analysis (GEPIA) tool and RT-PCR assays. The cell counting kit-8 (CCK-8) assays, transwell migration, and invasion assays were used for the functional study of cell viability, cell migration, and invasion. The influence of LINC00641 on cell cycle and apoptosis was determined using Flow cytometry detection. The regulating associations between LINC00641, miR-378a, and ZBTB20 were investigated in AML cells using the Luciferase reporter assays and RT-PCR assays RESULTS: We found that LINC00641 was highly expressed in AML specimens and cell lines. Functionally, the silence of LINC00641 inhibited the proliferation, migration, invasion, and cell cycle arrest in AML cells while inducing their apoptosis. The results using bioinformatics assays predicted the complementary binding sites within LINC00641 and miR-378a, which was demonstrated by the use of the Luciferase reporter assays. In addition, we also demonstrated that ZBTB20 was a direct target of miR-378a. Moreover, the inhibition of miR-378a could rescue the ZBTB20 protein level decrease induced by LINC00641 knockdown. CONCLUSIONS: We firstly identified LINC00641 as a novel AML-related lncRNA whose knockdown inhibited cell proliferation, migration, invasion, and promoted apoptosis by modulating miR-378a/ZBTB20 axis in AML.