This product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human TE1 cell line, engineered to disrupt the ABCB10 gene. ABCB10 encodes a mitochondrial inner membrane ATP-binding cassette transporter critical for heme biosynthesis and iron-sulfur (Fe-S) cluster assembly. The polyclonal knockout pool is generated using non-homologous end joining repair following Cas9-mediated double-strand breaks, resulting in a heterogeneous loss-of-function model suitable for studying gene function without single-cell clonal selection. This approach provides a robust cellular system for investigating mitochondrial iron metabolism, oxidative stress responses, and apoptosis regulation in an esophageal squamous cell carcinoma background.
TE1 cells were originally established from a primary esophageal squamous cell carcinoma of a female patient and exhibit a well-differentiated epithelial phenotype. This cell line retains key genomic and signaling features of esophageal squamous cell carcinoma, including alterations in cell cycle control and apoptotic pathways. TE1 cells are widely employed as a model for studying esophageal cancer biology, therapeutic resistance, and mitochondrial function. The well-differentiated nature of TE1 cells makes them particularly useful for examining how ABCB10 knockout influences processes such as heme synthesis and redox homeostasis in a context that closely mirrors the tissue of origin, providing disease-relevant insights for esophageal oncology research.
ABCB10 functions as a mitochondrial inner membrane transporter, facilitating the export of heme or its biosynthetic intermediates into the cytoplasm. This activity is essential for coordinating heme production with Fe-S cluster assembly, as ABCB10 directly interacts with ferrochelatase (FECH) and ABCB7 within the mitochondrial matrix. Transcription of ABCB10 is positively regulated by GATA1 and NRF2 under conditions of oxidative stress, while HIF1?? can modulate its expression during hypoxia. At the protein level, ABCB10 associates with mitoferrin and mitofilin to maintain mitochondrial iron homeostasis and cristae structure. Disruption of ABCB10 leads to impaired heme synthesis, defective Fe-S cluster biogenesis via ISCU and frataxin (FXN), and loss of mitochondrial superoxide dismutase (SOD2) activity. This results in elevated mitochondrial reactive oxygen species (ROS), diminished anti-apoptotic signaling through BCL2, and enhanced BAX-mediated apoptosis, underscoring ABCB10??s role in redox detoxification and cell survival.
In the esophageal squamous cell carcinoma context, ABCB10 loss-of-function models are highly relevant for dissecting mechanisms of drug resistance and apoptosis evasion. Esophageal cancers often exhibit altered mitochondrial metabolism and heightened oxidative stress tolerance, processes in which ABCB10 is centrally involved. The knockout of ABCB10 in TE1 cells perturbs heme-dependent functions and Fe-S cluster delivery to respiratory chain complexes, rendering cells more susceptible to oxidative damage and pro-apoptotic stimuli. This system enables researchers to examine how mitochondrial iron handling intersects with tumor cell fitness, and how impairment of the ABCB10-dependent pathway may be exploited to sensitize carcinoma cells to conventional chemotherapeutics or targeted agents, particularly those inducing ROS or interfering with BCL2-regulated apoptosis.
This polyclonal knockout cell product is designed for a wide range of research applications, including mitochondrial iron homeostasis studies, oxidative stress response analysis, and apoptosis signaling investigation. Representative assays include western blotting and RT-qPCR to confirm gene disruption and downstream target expression changes, Seahorse metabolic flux analysis to assess mitochondrial respiration, mitochondrial membrane potential and ROS detection assays, and cell proliferation or drug sensitivity assays for evaluating resistance mechanisms. The model is also suitable for ABCB10 inhibitor screening and functional rescue experiments. For additional technical information or to inquire about lot-specific details, please contact Ascent Research.
