Pseudogene PA2G4P4 promotes oncogene PA2G4 expression and nuclear translocation to affect glioblastoma cell viability and apoptosis.

Dysregulation of pseudogenes is involved in the progression of various types of cancer, including glioblastoma (GBM). Proliferation associated-2G4 (PA2G4) pseudogene 4 (PA2G4P4) has been shown to play an oncogenic role in bladder cancer development. Our study aimed to explore the role and mechanism of PA2G4P4 in GBM progression. PA2G4P4 and PA2G4 expression in GBM tissues was analyzed using the GEPIA database. Cell viability, apoptosis, and activities of caspase-3 and caspase-9 in GBM cells were explored by CCK-8, flow cytometry analysis, and colorimetric activity assay kits, respectively. GEPIA database showed that PA2G4P4 and PA2G4 were both upregulated in GBM tissues. PA2G4P4 expression was also boosted in GBM cells. Knockdown of PA2G4P4 or PA2G4 inhibited cell viability, induced apoptosis, and increased caspase-3 and caspase-9 activities in GBM cells. Data from UALCAN database showed that among top 15 genes correlated with PA2G4P4, PA2G4 had the highest correlation coefficient. Additionally, knockdown of PA2G4P4 inhibited PA2G4 expression and nuclear translocation in GBM cells. Overexpression of PA2G4 abolished the functions of PA2G4P4 knockdown on viability and apoptosis in GBM cells. Summarily, pseudogene PA2G4P4 promotes oncogene PA2G4 expression and nuclear translocation to affect cell viability and apoptosis in GBM cells.

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