The AIFM2 Knockout LoVo Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population targeting the AIFM2 gene (also known as FSP1) in the human LoVo colon adenocarcinoma cell line. This gene-disrupted polyclonal pool enables loss-of-function studies of AIFM2 in colorectal cancer models. As a polyclonal product, it retains the genetic heterogeneity of the edited population, providing a robust tool for functional genomics without single-cell cloning artifacts.
The LoVo cell line is derived from a metastatic colon adenocarcinoma (Dukes’ type C) of a 56-year-old Caucasian male, and serves as a well-established tumorigenic model for colorectal cancer research. These epithelial cells maintain key oncogenic features, including KRAS and TP53 mutations, and are widely used to investigate metastatic progression, drug resistance, and signal transduction pathways. Their adherent growth and reproducible behavior in xenograft and in vitro assays make them a reliable platform for dissecting colorectal cancer biology.
AIFM2 encodes a mitochondrial oxidoreductase that acts as a ferroptosis suppressor independent of GPX4 by reducing coenzyme Q10 (CoQ10) to ubiquinol, a lipophilic radical-trapping antioxidant that prevents lipid peroxidation. Its expression is regulated by TP53 and NFE2L2 (NRF2) under oxidative stress, and it interacts with CoQ10, NAD(P)H, and Bcl-2 family proteins, also contributing to caspase-independent apoptosis. AIFM2 operates in parallel with the SLC7A11?CGPX4 axis and modulates ACSL4-dependent lipid metabolism, underscoring its pivotal role in redox homeostasis.
In colorectal cancer, ferroptosis evasion is a recognized mechanism of drug resistance and tumor progression. AIFM2 overexpression has been observed in certain drug-resistant cancer cells, making its knockout in LoVo cells a valuable system for studying ferroptosis sensitization. This model allows researchers to dissect how AIFM2 loss influences lipid peroxidation, apoptotic cross-talk, and sensitivity to ferroptosis inducers such as erastin and RSL3. Given the tumorigenic background of LoVo cells, this knockout pool is particularly suited for exploring the interplay between ferroptosis, oxidative stress, and oncogenic signaling in colorectal carcinoma.
Typical applications include ferroptosis mechanism studies using Western blotting for GPX4, ACSL4, and lipid peroxidation markers, lipid peroxidation assays with C11-BODIPY, and cell viability assays with erastin or RSL3. RT-qPCR confirms AIFM2 knockdown, and clonogenic survival assays assess long-term effects. Flow cytometry for apoptosis and drug sensitivity profiling further explore ferroptosis?Capoptosis crosstalk. This polyclonal model is a versatile tool for redox biology, drug screening, and colorectal cancer resistance research. For more information, please contact Ascent Research.
