the_cancer_genome_atlas_glioblastoma_multiforme [Neurosurgery Wiki]

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[[Gene expression analysis]] was performed in Glioblastoma tumor samples and normal controls from [[Kunming]], [[The Cancer Genome Atlas Glioblastoma Multiforme]] ([[TCGA-Glioblastoma]]) cohort, and the [[Gene Expression Omnibus]] (GEO) database (GSE7696). [[Cell proliferation]], [[apoptosis]], Matrigel Transwell, colony formation, and cell cycle assays were performed in T98 G and U251 cells in vitro. An orthotopic U251 xenograft murine model was employed to test the effects of RP3-439F8.1 knockdown in vivo.

[[NR5A2]] was upregulated in the three independent Glioblastoma tumor cohorts. [[In vitro]], NR5A2 overexpression enhanced Glioblastoma cell proliferation, colony formation, invasiveness, and G0-G1 cell cycle phase shift via co-activating β-catenin/TCF4 signaling, with no apparent effect upon apoptosis. In contrast, RP3-439F8.1 knockdown produced the opposite effects. RP3-439F8.1 knockdown reduced tumor progression in vivo, increasing overall survival in model mice. Further in vitro experiments revealed that RP3-439F8.1 acts as a competing endogenous RNA (ceRNA) to regulate NR5A2 by sponging the microRNA miR-139-5p. These findings were clinically validated by a positive correlation between RP3-439F8.1 and NR5A2 and a negative correlation between RP3-439F8.1 and miR-139-5p in Glioblastoma tumors.

The study supports a tumorigenic role for RP3-439F8.1 in Glioblastoma through the RP3-439F8.1/miR-139-5p/NR5A2 axis
((Qi J, Pan L, Yu Z, Ni W. The [[lncRNA]] [[RP3-439F8.1]] promotes Glioblastoma [[cell proliferation]] and progression by sponging [[miR-139-5p]] to upregulate [[NR5A2]]. Pathol Res Pract. 2021 Jan 2;223:153319. doi: 10.1016/j.prp.2020.153319. Epub ahead of print. PMID: 33991848.))