The AIFM2 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human esophageal squamous cell carcinoma line KYSE-150. This polyclonal population harbors diverse disruptive edits in the AIFM2 gene, enabling loss-of-function studies while avoiding clonal selection bias. Researchers can use this model to investigate the tumor-suppressive roles of AIFM2 and its contributions to cell death regulation.
KYSE-150 is a widely used human esophageal squamous cell carcinoma cell line originally derived from a primary tumor of a Japanese female patient. These cells exhibit characteristic epithelial morphology and retain key molecular features of esophageal malignancies, including altered p53 signaling and susceptibility to oxidative stress. The line serves as a physiologically relevant platform for studying cancer biology, particularly the molecular mechanisms underlying esophageal carcinogenesis and therapeutic resistance.
AIFM2 encodes an NAD(P)H-dependent oxidoreductase with dual roles in cell fate. Upon genotoxic stress, it translocates to the nucleus to induce caspase-independent apoptosis, a process regulated by p53. Concurrently, AIFM2 localizes to mitochondria and the plasma membrane to protect cells from ferroptosis by reducing lipid peroxides and lowering mitochondrial reactive oxygen species. It interacts with mitochondrial respiratory chain complexes and lipid peroxides, bridging redox balance and cell survival. AIFM2 expression is induced by p53 and modulated by ferroptosis inducers such as erastin, positioning it at the intersection of apoptosis and ferroptosis pathways.
In KYSE-150 cells, which harbor a mutation-prone esophageal tumor background, disruption of AIFM2 allows dissection of its tumor-suppressive functions. The knockout model can reveal how loss of AIFM2-mediated ferroptosis protection or apoptosis induction affects esophageal cancer cell viability, proliferation, and response to chemotherapeutic agents. Given the frequent dysregulation of p53 in esophageal squamous cell carcinoma, this tool enables examination of the p53-AIFM2 axis in a disease-relevant setting. Moreover, it provides a platform to study metabolic vulnerabilities and mitochondrial dysfunction associated with AIFM2 deficiency.
This polyclonal knockout cell product is ideally suited for a range of experimental applications. Researchers can assess apoptotic susceptibility via Annexin V staining and flow cytometry following treatment with genotoxic agents like etoposide. Ferroptosis regulation can be examined through erastin-induced cell death and rescue experiments, coupled with lipid peroxidation assays using C11-BODIPY. Mitochondrial membrane potential can be monitored with JC-1 staining, and drug sensitivity screens can identify compounds that exploit AIFM2 loss. Additional techniques such as western blotting, RT-qPCR, and immunofluorescence are essential for target validation. For further inquiries, please contact Ascent Research.
