The ABCB10 Knockout UM-UC-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for precise disruption of the ABCB10 gene in the human bladder cancer cell line UM-UC-3. This product provides a heterogeneous pool of edited cells with loss-of-function mutations in ABCB10, enabling robust study of the gene’s role in mitochondrial iron metabolism and redox homeostasis without the need for single-cell cloning. The polyclonal format preserves biological variability while maintaining a consistent knockout background, making it suitable for functional genomics, pharmacological profiling, and mechanistic investigations in cancer biology.
The host cell line, UM-UC-3, is a well-characterized transitional cell carcinoma line originating from a male patient with bladder cancer. As a model system, UM-UC-3 cells exhibit key features of urothelial carcinoma, including invasive potential and relevant molecular signaling pathways, thus serving as a physiologically relevant platform to interrogate the consequences of ABCB10 ablation in the context of bladder tumor biology. This cellular background is particularly advantageous for studying mitochondrial adaptations and stress responses in urothelial malignancies.
ABCB10 encodes a mitochondrial inner membrane ATP-binding cassette transporter essential for heme biosynthesis and iron-sulfur cluster export. It homodimerizes and interacts with Mitoferrin-1 and Ferrochelatase, facilitating iron incorporation into heme. ABCB10 transcription is regulated by GATA1, NRF2, STAT3, TFCP2, and CP2. Following gene disruption, Ferrochelatase activity is compromised, reducing heme production, increasing reactive oxygen species, and dysregulating iron homeostasis. Hemoprotein maturation??including cytochromes??is impaired, crippling oxidative phosphorylation and elevating oxidative stress.
In UM-UC-3 cells, ABCB10 knockout creates a bladder cancer model for studying mitochondrial iron metabolism and its role in tumor biology. Loss of ABCB10 perturbs heme and iron-sulfur cluster synthesis, potentially sensitizing cells to ferroptosis. This model enables investigation of metabolic vulnerabilities in bladder cancer and can identify therapeutic targets that exploit mitochondrial dysfunction, as well as explore ABCB10’s role in chemoresistance and tumor growth.
Researchers can use this polyclonal knockout population for Western blotting, RT-qPCR, heme quantification, cellular iron measurement, ROS detection, lipid peroxidation assays, cell viability and caspase activation assays, wound healing migration assays, and xenograft tumor growth studies. It is also suitable for drug screening to identify ferroptosis inducers or metabolic modulators. For further information, please contact Ascent Research.
