The ABCB10 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of HCT 116 colorectal carcinoma cells, in which the ABCB10 gene has been disrupted to establish a loss-of-function model. This product preserves the parental line’s epithelial characteristics while enabling investigation of mitochondrial iron homeostasis, heme biosynthesis, and oxidative stress management. The polyclonal format encompasses diverse gene-editing events, making the population well-suited for pooled functional studies without clonal selection.
The HCT 116 host cell line is a human colorectal carcinoma epithelial model with microsatellite instability-high (MSI-H) due to MLH1 deficiency and wild-type p53. Widely used in cancer research, it provides a well-characterized platform for studying tumorigenesis, DNA mismatch repair, and drug responses, ensuring reproducibility in gene-editing experiments.
ABCB10 is a mitochondrial ATP-binding cassette transporter that facilitates iron-sulfur cluster biogenesis and heme production. It operates downstream of transcription factors GATA1 and NRF2 and directly associates with ferrochelatase (FECH) and mitoferrin-1 (SLC25A37) to maintain mitochondrial iron homeostasis and mitigate reactive oxygen species (ROS) accumulation. ABCB10 disruption impairs this network, leading to elevated ROS, loss of mitochondrial membrane potential, and enhanced sensitivity to ferroptosis through deregulation of GPX4 and SLC7A11.
In the HCT 116 context, ABCB10 knockout creates a valuable tool for studying mitochondrial iron metabolism in colorectal cancer. The cell line’s intact p53 and MSI-H status enable investigation of how ABCB10 loss affects apoptosis, ferroptosis, and survival pathways, highlighting metabolic weaknesses that could be exploited therapeutically. This model is especially relevant for assessing the role of mitochondrial dysfunction in tumorigenic epithelial cells.
Applications include exploring mitochondrial iron trafficking, ferroptosis induction using erastin or RSL3, and oxidative stress responses via MitoSOX. Standard assays such as Western blotting for ABCB10 and FECH, Annexin V/PI apoptosis detection, MTT viability assays, and immunofluorescence can be employed. The polyclonal nature supports pooled functional screening and drug response evaluation in colorectal cancer research. For ordering and technical support, please contact Ascent Research.
