Background
Glioblastoma has been seen as the most common malignancy of brain tumor. Emerging reports has claimed that SNHG29 (LRRC75A-AS1) was involved in several biological processes via modulation of signaling pathway, and served as an malignant facilitatorin osteosarcoma. However, the specific role of SNHG29 in glioblastoma remains unknown.
Conclusions
In conclusion, SNHG29 regulates miR-223-3p/CTNND1 axis to promote glioblastoma progression via Wnt/β-catenin signaling pathway, offering a potential therapeutic point for glioblastoma patients.
Methods
RT-qPCR and microarray were operated to measure genes expression. Western blot was performed to examine protein expression. CCK-8 and colony formation assays were used to evaluate cell proliferation. Cell migration was tested by transwell assay. Nuclear-cytoplasmic fractionation was conducted to locate SNHG29. The binding capacity of miR-223-3p to SNHG29 or CTNND1 3'UTR was verified by RIP and luciferase reporter assay.
Results
SNHG29 presented high expression in glioblastoma to boost cell proliferation, migration and EMT process. In addition, miR-223-3p was validated to bind with SNHG29 after prediction and screening. Furthermore, miR-223-3p was proved to be a negative regulator for its target CTNND1. Then, the inhibition on cell proliferation, migration and EMT process resulted from SNHG29 knockdown was recovered by CTNND1 overexpression. At last, the inhibitive impacts on cell proliferation, migration and EMT process of CTNND1 deficiency was abrogated by LiCl. Conclusions: In