Description

TP53 Knockout A-172 Cell Line is a CRISPR/Cas9-engineered human glioblastoma astrocytoma-derived cell model in which the TP53 locus has been disrupted to eliminate functional p53 expression. This stable in vitro knockout system is generated in A-172 cells, an epithelial-like adherent CNS glial tumor cell line, and provides a defined platform for investigating loss of TP53-dependent stress signaling in a malignant astrocytic cellular background.

A-172 cells are widely used as a human brain tumor model for studies of proliferation, survival signaling, DNA damage responses, and anticancer drug sensitivity. Because they are derived from glioblastoma/astrocytoma, they are relevant for experimental interrogation of tumor-associated pathways operating in malignant glial cells, including checkpoint regulation, apoptosis control, metabolic adaptation, and therapy response. Their established use in adherent culture also supports mechanistic studies that integrate molecular profiling with phenotypic assays relevant to glioblastoma biology and broader solid tumor research.

TP53 encodes p53, a stress-responsive tumor suppressor transcription factor activated by DNA damage, oncogenic stress, and hypoxia. In canonical signaling, p53 is regulated upstream by ATM and ATR, with downstream CHEK1 and CHEK2 signaling contributing to p53 activation, while MDM2 and MDM4 mediate inhibitory control over p53 stability and activity. ARF/CDKN2A can counteract MDM2-dependent suppression, further linking TP53 to oncogene-induced stress pathways. p53 interacts with cofactors and signaling components including EP300/p300, CREBBP/CBP, TP53BP1, and the RNA polymerase II transcriptional machinery to drive transcriptional programs that promote expression of CDKN1A/p21, BAX, BBC3/PUMA, PMAIP1/NOXA, GADD45A, FAS, APAF1, and MDM2. Through these outputs, TP53 acts upstream of cell-cycle arrest, intrinsic apoptosis, senescence, DNA repair, and metabolic regulation, and its disruption is strongly relevant to glioblastoma, Li-Fraumeni syndrome-associated biology, therapy resistance, and genomic instability research.

In the A-172 background, TP53 knockout enables direct analysis of how p53 loss reshapes glioblastoma-associated stress responses and checkpoint control. This model is useful for examining altered induction of canonical p53 target genes after irradiation, genotoxic challenge, or oncogenic stress, and for assessing how TP53 deficiency influences survival signaling, apoptotic priming, senescence-associated phenotypes, and pathway dependence in tumor-derived glial cells.

Researchers can apply this cell line in western blotting, RT-qPCR, and RNA-seq workflows to quantify loss of TP53-regulated transcriptional responses; in flow cytometry cell-cycle analysis to examine checkpoint defects; and in apoptosis assays, clonogenic survival assays, and drug sensitivity studies to characterize resistance or vulnerability under chemotherapy or radiation exposure. Additional applications include immunofluorescence analysis of DNA damage foci, reporter assays for p53-responsive transcription, co-immunoprecipitation to study interactions involving MDM2 or TP53BP1-associated signaling networks, and phospho-signaling analysis of ATM/ATR-CHEK pathway engagement in the absence of functional p53. Researchers may contact Ascent Research for additional technical information, product details, or related gene-edited cell models.