The ABCB10 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human KYSE-150 esophageal squamous cell carcinoma line. Generated by CRISPR/Cas9-mediated gene disruption, this product contains a heterogeneous mixture of cells carrying loss-of-function mutations in ABCB10. The polyclonal format avoids clonal selection biases and is well-suited for pooled screening applications and population-level functional analyses.
KYSE-150 is a poorly differentiated esophageal squamous cell carcinoma line harboring a TP53 mutation, which abrogates p53-mediated tumor suppression and contributes to genomic instability and altered apoptosis regulation. This established model is widely used to study ESCC tumorigenesis, metastasis, and therapeutic responses, rendering it a relevant host for investigating the impact of mitochondrial transporter dysfunction in cancer.
ABCB10 encodes a mitochondrial inner membrane transporter critical for heme biosynthesis and iron homeostasis. It functions alongside mitoferrin-1 (SLC25A37) and ferrochelatase (FECH), and is transcriptionally controlled by GATA1, HIF1A, and NRF2. ABCB10 supports mitochondrial iron-sulfur cluster biogenesis, heme export, and ROS modulation, while influencing apoptosis regulators of the BCL2 family. Pathway components such as ALAS2, SOD2, and GPX4 intersect with its role in oxidative stress defense. CRISPR/Cas9-mediated knockout disrupts heme metabolism, alters mitochondrial iron trafficking, and sensitizes cells to oxidative damage and apoptosis.
In the TP53-mutant background, ABCB10 loss exacerbates mitochondrial liability and may reveal synthetic lethal interactions or therapeutic sensitivities. This model links mitochondrial transporter dysfunction to esophageal cancer progression and drug resistance, enabling dissection of how mitochondrial defects influence apoptotic thresholds and oxidative stress adaptation. It also provides a system for investigating mitochondrial diseases and sideroblastic anemia linked to defective heme or iron metabolism.
These polyclonal knockout cells are suitable for pooled CRISPR screen validation, mitochondrial biology investigations, and esophageal cancer drug resistance studies. Pooled screening enables systematic identification of genetic interactions, while assays such as western blotting, heme quantification, ROS detection (DCFDA), mitochondrial membrane potential (JC-1), and apoptosis (Annexin V/PI) facilitate functional characterization. Transcriptomic (RNA-seq) and gene expression (RT-qPCR) profiling complement these approaches. For further technical details and support, please contact Ascent Research.
