The HMOX1 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma cell line. This pool contains a heterogeneous mixture of cells with targeted disruptions in HMOX1, resulting in loss of heme oxygenase-1 function. The polyclonal format avoids clonal selection biases and provides a population-wide knockout effect.
The parental A-549 cell line was established from a 58-year-old male with lung adenocarcinoma and serves as a model for non-small cell lung cancer (NSCLC). These adherent epithelial cells retain characteristics of alveolar Type II pneumocytes and are widely utilized in studies of cancer biology, drug resistance, and oxidative stress.
HMOX1 encodes inducible heme oxygenase-1, which catalyzes the rate-limiting cleavage of heme into biliverdin, carbon monoxide (CO), and ferrous iron. This reaction is driven by NADPH and facilitated by the interaction with cytochrome P450 reductase. Expression is predominantly regulated by the transcription factors Nrf2 and Bach1, responding to heme, oxidative stress, hypoxia, and cytokines such as TNF-?? and IL-10. Biliverdin is metabolized to bilirubin by biliverdin reductase, CO acts as a signaling molecule, and free iron induces ferritin synthesis. HMOX1 also promotes p21 expression, contributing to cell cycle control and ferroptosis resistance.
In A-549 lung adenocarcinoma cells, HMOX1 mediates cytoprotective and antioxidant responses critical for survival in the tumor microenvironment. Elevated HMOX1 expression is linked to chemoresistance and poor prognosis in NSCLC. Disruption of HMOX1 in this polyclonal knockout model sensitizes cells to ferroptosis inducers and ROS-generating agents, enabling the investigation of redox-dependent drug resistance and Nrf2-driven prosurvival signaling.
This product supports diverse assays such as western blotting, RT-qPCR, heme oxygenase activity measurements, ROS detection, and ferroptosis sensitivity profiling. It is ideal for studying heme catabolism, iron metabolism, anti-inflammatory signaling, and lung cancer biology. Co-culture and drug combination studies can further delineate HMOX1’s role in tumor-immune interactions and therapeutic vulnerabilities. For additional details, please contact Ascent Research.
