ABCB10 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the Huh-7 human hepatocellular carcinoma cell line with targeted disruption of the ABCB10 locus. This heterogeneous pool enables loss-of-function studies of the mitochondrial ABC transporter, avoiding clonal selection bias and reflecting the natural diversity of editing outcomes. Researchers can immediately use these cells to investigate mitochondrial transport and its role in disease-relevant pathways.
Huh-7 is a well-differentiated hepatoma cell line widely employed in liver cancer and hepatic metabolism research. These epithelial cells retain key hepatocellular functions, including lipoprotein synthesis and xenobiotic metabolism, while exhibiting malignant features. Their human origin and hepatic background make them an optimal host for generating knockout models that explore mitochondrial dysfunction and hepatocellular carcinoma pathogenesis.
ABCB10 encodes an inner mitochondrial membrane ABC transporter that exports heme or its biosynthetic intermediates, governing heme biosynthesis, iron homeostasis, and oxidative phosphorylation. Its expression is regulated by GATA1 and NF-E2, and it functionally cooperates with SLC25A37 (mitoferrin), ferrochelatase (FECH), and ALAS2. ABCB10 also contributes to cytochrome c assembly and iron?sulfur cluster biogenesis. Loss of ABCB10 disrupts heme trafficking, leading to heme precursor accumulation, heightened oxidative stress, compromised respiration, and increased apoptotic sensitivity.
In Huh-7 hepatocellular carcinoma cells, mitochondrial metabolism and iron handling are frequently dysregulated, supporting rapid proliferation and drug resistance. ABCB10 knockout disrupts heme export, undermining mitochondrial fitness, elevating reactive oxygen species, and potentially sensitizing cells to therapeutic agents such as sorafenib. This model therefore allows dissection of mitochondrial heme trafficking in liver tumor biology and evaluation of ABCB10 as a therapeutic vulnerability.
Applications include western blot analysis of heme synthesis enzymes, heme quantification, mitochondrial membrane potential assays (JC?1/TMRE), apoptosis detection (Annexin V), transcriptomic profiling by RNA?seq, and metabolic flux measurements via oxygen consumption rate (OCR). These approaches enable studies of heme metabolism, mitochondrial dysfunction, iron homeostasis, and drug sensitivity in liver cancer. For additional information or custom project inquiries, contact Ascent Research.
