Transcriptome analysis of TP53-R248L overexpressed 19NS patient-derived glioblastoma cells. Homo sapiens

This study demonstrates the role of TP53 gain-of-function (GOF) mutation on glioblastoma progression. However, little is known about the transcriptional alteration upon TP53 GOF mutation. In this study, we found that TP53 GOF mutation (R248L mutation) promotes the enrichment of multiple gene signatures related to inflammation and chemotaxis. Particularly, through in vitro and in vivo approaches, we verified that TP53 GOF mutation enhances NFKB signaling which in turn up-regulates CCL2 and TNFA. Taken together, these results suggest the function of TP53 GOF mutation driving aggressiveness of malignant brain tumor. Overall design: A patient-derived glioblastoma cell line 19NS was transfected with pLL CMV puro (19NS-control) or pLL CMV TP53-R248L puro (19NS-TP53-R248L). The 3 biological replicates of RNA extracts in these cells was used for transcriptome analysis.