LncRNA SNHG1 contributes to tumorigenesis and mechanism by targeting miR-338-3p to regulate PLK4 in human neuroblastoma.

OBJECTIVE

Neuroblastoma is a common malignancy in children. Despite the occurrence of diverse therapies in recent years, the survival rate of patients with high-risk NB is still unpredictable due to the high metastatic potential and poor prognosis. Therefore, it is urgent to study the molecular mechanism of NB metastasis. SNHG1 has been reported to be closely related to the development, metastasis, and prognosis of many cancers. The purpose of this study was to clarify the molecular mechanism of the role of SNHG1 in NB tumors.

PATIENTS AND METHODS

The expression levels of SNHG1, miR-338-3p, and PLK4 were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot, respectively. The functional targets between miR-338-3p and SNHG1 or PLK4 were predicted by online software Diana tools and observed by Luciferase reporter assay and RIP assay. Cell proliferation was measured by MTT assay. Cell migration and invasion were operated through flow cytometry. The expression of p-AKT was quantified by Western blot. Xenograft tumor model was established to confirm the biological role of SNHG1 in NB in vivo.

RESULTS

The expression levels of SNHG1 and PLK4 were increased in NB tissues and cells, and miR-338-3p expression was on the contrary. PLK4 was verified as a direct target of miR-338-3p and miR-338-3p could specially bind to SNHG1. The negative effect of SNHG1 down-regulation on cell proliferation, migration, and invasion could be rescued by miR-338-3p inhibition. The suppression of miR-338-3p mimics on cell proliferation, migration, and invasion could be reversed by PLK4 overexpression. In addition, SNHG1 knockdown weakened the volume and weight of tumor in vivo.

CONCLUSIONS

SNHG1 conduced to tumorigenesis and mechanism by upregulating PLK4 and by acting as miR-338-3p sponge in neuroblastoma.