The AIFM2 Knockout TE1 Polyclonal Cells product comprises a population of human TE1 esophageal squamous cell carcinoma cells genetically modified through CRISPR/Cas9-mediated disruption of the AIFM2 gene. This polyclonal knockout cell population provides a heterogeneous loss-of-function model system for investigating the functional role of AIFM2 in cellular processes. The gene-edited pool enables researchers to study the effects of AIFM2 deficiency without the biases associated with single-cell clonal isolation, suitable for functional assays requiring population-level responses.
The parental TE1 cell line is a well-characterized model of esophageal squamous cell carcinoma, derived from a primary human tumor. TE1 cells retain aberrant p53 signaling and dysregulated apoptotic pathways, providing a relevant platform for studying esophageal cancer biology and therapeutic responses. This cell line is extensively employed to investigate tumor proliferation, invasion, and sensitivity to DNA-damaging agents, and is valued for its ability to model p53-dependent and -independent death mechanisms.
AIFM2 (AMID) is a flavoprotein oxidoreductase and p53-inducible mitochondrial pro-apoptotic protein. Upon DNA damage, p53 activation transcriptionally upregulates AIFM2, which localizes to mitochondria before translocating to the nucleus. There, it interacts with DNA and nuclear matrix components to drive chromatin condensation and large-scale DNA fragmentation independently of caspases. This pathway operates downstream of p53 and functionally converges with BAX and cytochrome c release, yet proceeds without caspase involvement. Disruption of AIFM2 expression in these polyclonal knockout cells enables dissection of this non-canonical apoptotic branch.
In esophageal squamous cell carcinoma, AIFM2-mediated cell death is a critical tumor-suppressive mechanism often inactivated during cancer progression. Loss of AIFM2 can promote resistance to chemotherapy and radiation. This knockout model facilitates the study of how TE1 cells evade p53-dependent apoptosis and identifies alternative survival pathways. It is valuable for evaluating the requirement of AIFM2 for drug sensitivity and for exploring mitochondrial dysfunction-associated cell death.
These polyclonal AIFM2 knockout cells are applicable to diverse assays: western blotting and RT-qPCR for gene and protein expression analysis; immunofluorescence for AIFM2 localization; TUNEL and Annexin V staining for apoptosis assessment; and flow cytometry for mitochondrial membrane potential and cell death. Researchers can use the model to validate CRISPR screens, investigate p53 signaling dynamics, or screen compounds that restore caspase-independent cell death. Sanger sequencing enables confirmation of population-level editing. They also serve as a companion tool for in vivo xenograft studies examining AIFM2’s role in tumor suppression. For technical inquiries, contact Ascent Research.
