AIFM2 Knockout SK-OV-3 Polyclonal Cells are a heterogeneous cell population generated by CRISPR/Cas9-mediated gene disruption of the AIFM2 locus in the SK-OV-3 human ovarian adenocarcinoma cell line. This polyclonal knockout product encompasses a range of loss-of-function alleles, providing a robust model for studying AIFM2-dependent processes without clonal selection bias.
The host SK-OV-3 cell line is a human ovarian adenocarcinoma epithelial model established from a malignant ascites. These cells exhibit inherent chemoresistance, likely due to multiple survival mechanisms, and offer a clinically relevant platform for exploring ovarian cancer biology and therapeutic vulnerabilities.
AIFM2 encodes a mitochondrial oxidoreductase with dual roles: as apoptosis-inducing factor 2, it promotes caspase-independent programmed cell death by translocating to the nucleus and inducing large-scale DNA fragmentation, a process transcriptionally activated by TP53 and E2F1 in response to DNA damage or oxidative stress. As ferroptosis suppressor protein 1 (FSP1), AIFM2 reduces coenzyme Q10 to ubiquinol at the plasma membrane, thereby intercepting lipid peroxyl radicals and inhibiting ferroptosis independently of GPX4. This function positions AIFM2 as a critical node where apoptosis and ferroptosis pathways converge, interacting with BCL2 family members such as BCL2 and BCL-XL.
In the chemoresistant SK-OV-3 background, AIFM2 knockout permits direct investigation of its dual role in apoptosis induction and ferroptosis suppression. Ablation of AIFM2 disrupts the FSP1?CCoQ10 axis, rendering cells more vulnerable to ferroptosis induction by erastin or class I ferroptosis inducers, while also impairing the caspase-independent apoptotic pathway. This model is thus suited for dissecting the ferroptosis?Capoptosis crosstalk and for screening agents that exploit oxidative stress vulnerabilities in ovarian cancer. The polyclonal nature maintains genetic diversity, reflecting the heterogeneity of tumors and facilitating robust pharmacological studies.
Key research applications include characterizing the p53-AIFM2-FSP1 signaling axis, elucidating ferroptosis resistance mechanisms, evaluating chemosensitizing strategies, and performing drug combination screens. Representative assays comprise Western blotting and RT-qPCR for AIFM2 and GPX4 expression levels, Annexin V apoptosis assays, caspase-3/7 activity measurements, lipid peroxidation assessment via C11-BODIPY staining, and co-immunoprecipitation to probe AIFM2 interactions with BCL2 or BCL-XL. Additionally, cell viability and migration/invasion assays under cisplatin or doxorubicin treatment can reveal AIFM2-dependent therapeutic responses. For detailed information and ordering, please contact Ascent Research.
