Background
The
Conclusion
FOXD3-AS1 promoted the tumorigenesis of glioma, and exerted its function to modulate SZRD1 by targeting miR-128-3p.
Methods
The FOXD3-AS1 expression and its prognostic relation were detected by bioinformatics tool. Next, glioma cell lines (HS683, U251, T98G, and SNB-19) were used to verify the FOXD3-AS1 expression. Furthermore, the roles of the FOXD3-AS1/miR-128-3p/SZRD1 axis on the glioma development in vitro and in vivo were examined.
Results
Bioinformatics analysis showed that FOXD3-AS1 was upregulated in the glioma and linked with poor prognosis. Consistently, FOXD3-AS1 level was overexpressed in the glioma cell lines (HS683 and U251). Subsequently, we verified that silencing of FOXD3-AS1 (si-FOXD3-AS1) restrained the cell proliferation, invasion, and tumor growth in vivo, and induced G0/G1 arrest, and promoted apoptosis. Further study also stated that FOXD3-AS1 interacted with miR-128-3p and SZRD1 was the target gene of miR-128-3p. Moreover, overexpression of miR-128-3p restrained the cell proliferation and metastasis of glioma, and reduced the SZRD1 level. Rescue assay illustrated that miR-128-3p inhibitor could reverse the suppressive impact of si-FOXD3-AS1 on the glioma progression. Similarly, SZRD1 overexpression could neutralize the influences of miR-128-3p mimic on glioma progression.