The AIFM2 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of the human osteosarcoma 143B cell line, featuring targeted disruption of the AIFM2 gene. This product provides a heterogeneous loss-of-function model for studying AIFM2, also known as ferroptosis suppressor protein 1 (FSP1), without clonal selection. The polyclonal approach maintains population-level genetic variability relevant to tumor biology and facilitates functional genomics and drug target validation.
143B cells serve as a classic osteosarcoma model widely employed in mitochondrial research due to their dependence on oxidative metabolism and well-characterized mitochondrial physiology. These characteristics make them an optimal host for investigating AIFM2, which localizes to mitochondria and regulates redox homeostasis, apoptosis, and ferroptosis.
AIFM2 is a mitochondrial oxidoreductase that suppresses ferroptosis by reducing coenzyme Q10 to ubiquinol, which traps lipid peroxyl radicals independently of the GPX4 pathway. Upon lethal signals, AIFM2 is released from mitochondria and translocates to the nucleus, inducing chromatin condensation and DNA fragmentation as a caspase-independent apoptosis effector. Upstream regulators include TP53 and oxidative stress; downstream, AIFM2 loss promotes mitochondrial membrane potential loss, reactive oxygen species accumulation, and ferroptosis execution. It interacts with BCL2 family proteins and functions alongside GPX4, AIF, and caspases.
In the 143B osteosarcoma background, AIFM2 knockout enhances ferroptosis sensitivity and disrupts apoptosis regulation, providing a powerful platform to dissect therapy resistance mechanisms. Osteosarcoma cells exhibit elevated oxidative burden and altered apoptotic thresholds, making AIFM2 loss instrumental for studying mitochondrial quality control, lipid peroxidation dynamics, and cell population survival. The polyclonal nature mirrors intratumoral heterogeneity, offering translational insights into how AIFM2 dysfunction influences cancer cell fate.
This model is ideally suited for ferroptosis assays using lipid peroxidation probes such as C11-BODIPY, apoptosis detection, western blotting, and cell viability assessments under oxidative challenge. Additional applicable techniques include reactive oxygen species quantification, mitochondrial membrane potential measurement with dyes like JC-1, and co-immunoprecipitation to probe AIFM2 protein complexes. These applications extend to cancer therapy resistance, neurodegeneration, and ischemia-reperfusion injury research. For further information, please contact Ascent Research.
