The TP53 Knockout T98G Cell Line is a CRISPR/Cas9-edited knockout cell line offering a loss-of-function model of the TP53 tumor suppressor gene in human T98G glioblastoma cells. This engineered cell line facilitates studies of p53-dependent pathways and their perturbation in cancer biology. Disruption of TP53 eliminates functional protein expression, enabling precise dissection of its transcriptional and tumor-suppressive functions.
T98G cells, derived from a 61-year-old White male with glioblastoma multiforme, are a well-established model of glioblastoma. These cells display hallmark features of the disease, including dysregulated growth signaling and genomic instability, making them a relevant system for investigating brain tumor biology and therapeutic resistance.
TP53 encodes a transcription factor pivotal to the cellular stress response. Upon DNA damage or oncogenic stress, upstream kinases ATM, ATR, and DNA-PK phosphorylate and activate p53. Activated p53 transcriptionally regulates downstream targets such as CDKN1A (p21), BAX, and PUMA (BBC3), thereby inducing cell cycle arrest, apoptosis, or senescence. Negative regulation occurs through MDM2-mediated ubiquitination, while cofactors like p300/CBP and interacting partners such as 14-3-3 proteins modulate its function. These interactions place p53 at the center of key networks including the p53 signaling pathway and the DNA damage response, with cross-talk to the PI3K/AKT/mTOR pathway.
Knocking out TP53 in T98G cells disrupts these critical checkpoints, impairing DNA damage responses and promoting genomic instability. Loss of p53-mediated cell cycle arrest and apoptosis allows cells to evade growth control, mirroring the frequent TP53 mutations observed in glioblastoma. This model is thus instrumental for studying p53-dependent tumor suppression, drug resistance mechanisms, and the molecular basis of glioblastoma progression.
The TP53 Knockout T98G Cell Line supports diverse research applications, including cancer biology, drug resistance profiling, and DNA damage response studies. Compatible assays include western blotting, RT-qPCR, immunofluorescence, Annexin V apoptosis assays, flow cytometric cell cycle analysis, colony formation, xenograft tumor models, and drug sensitivity testing. For further details, please contact Ascent Research.
