Long non‐coding RNA ASBEL promotes osteosarcoma cell proliferation, migration, and invasion by regulating microRNA‐21

Osteosarcoma is the most common malignant bone tumor in children and adolescents with high rate of incidence, high frequency of recurrence, and high degree of metastasis. This study aimed to investigate the effects of long noncoding RNA antisense ncRNA in the abundant in neuroepithelium area (ANA)/B‐cell translocation gene 3 (BTG3) locus (lncRNA ASBEL) on the pathogenesis of osteosarcoma. The expression levels of ASBEL in human osteoblast cells and human osteosarcoma cells were evaluated using qRT‐PCR. Effects of ASBEL knockdown on cell viability, migration, and invasion were detected using trypan blue exclusion assay, cell migration, and cell invasion assay, respectively. The regulatory effects of ASBEL on microRNA‐21 (miR‐21) were analyzed using qRT‐PCR. The roles of miR‐21 and protein phosphatase 2A (PP2A), the possible downstream factor of miR‐21, in osteosarcoma cell proliferation, migration, and invasion were also explored. The results showed that ASBEL was highly expressed in osteosarcoma cells. Knockdown of ASBEL inhibited osteosarcoma cell viability, migration, and invasion, as well as the expression level of miR‐21. PP2A was a direct target of miR‐21, which participated in the effects of ASBEL and miR‐21 on the activation of phosphatidylinositol 3‐kinase/protein kinase 3/glycogen synthase kinase‐3β (PI3K/AKT/GSK3β) and mitogen‐activated protein kinase/extracellular regulated protein kinase (MEK/ERK) signaling pathways as well as the enhancement of osteosarcoma cell proliferation, migration, and invasion. In conclusion, we verified that ASBEL‐miR‐21‐PP2A pathway might play critical regulatory effects on the pathogenesis of osteosarcoma and could be as the potential therapeutic target and biomarker for osteosarcoma treatment. ASBEL was highly expressed in osteosarcoma cells. Knockdown of ASBEL inhibited osteosarcoma cell viability, migration, and invasion, as well as the expression level of miR‐21. PP2A was a direct target of miR‐21, which was participated in the effects of ASBEL and miR‐21 on the activation of phosphatidylinositol 3‐kinase/protein kinase 3/glycogen synthase kinase‐3β (PI3K/AKT/GSK3β) and mitogen‐activated protein kinase/extracellular regulated protein kinase (MEK/ERK) signaling pathways as well as the enhancement of osteosarcoma cell proliferation, migration, and invasion.