The HMOX1 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Ca Ski cervical carcinoma line, providing targeted disruption of the heme oxygenase-1 (HMOX1) gene. As a heterogeneous knockout pool, this model avoids clonal artifacts and is suitable for studying loss-of-function effects in a physiologically relevant tumor context.
The Ca Ski line is an adherent, HPV16-positive cervical carcinoma epithelial model. Constitutive expression of E6 and E7 oncoproteins inactivates p53 and Rb, respectively, driving tumorigenesis through deregulated proliferation, apoptosis resistance, and altered stress responses. This background recapitulates key features of HPV-associated cervical carcinogenesis.
HMOX1 encodes HO-1, the rate-limiting heme degradation enzyme producing biliverdin, CO, and Fe2?. Its transcription is activated by NRF2 via antioxidant response elements during oxidative stress, while Bach1 represses basal expression. Upstream signals include heme, MAP kinases (ERK, JNK, p38), PI3K/AKT, STAT3, NF-??B, and HIF-1??. Downstream, BLVRA reduces biliverdin to bilirubin, and ferritin is co-induced for iron sequestration. HO-1 modulates ferroptosis sensitivity and redox homeostasis.
In HPV16-driven cervical carcinoma, HMOX1 knockout allows dissection of HO-1 contributions to cell survival under oxidative load, iron handling, and chemoresistance. Loss of HO-1 may potentiate ferroptosis and impair the antioxidant defense co-opted by E6/E7. The model helps clarify intersections between viral oncoproteins and the NRF2?CBach1 stress axis.
Applications include western blotting (HO-1, NRF2, ferritin), RT-qPCR (HMOX1, HMOX2), enzyme activity and bilirubin assays, ROS detection (DCFDA), ferroptosis induction (erastin), viability under H?O? challenge, immunofluorescence, ARE reporter assays, and co-immunoprecipitation for NRF2/Bach1. This polyclonal knockout population supports research in cervical cancer redox biology, heme metabolism, ferroptosis, and anti-inflammatory mechanisms. Inquiries may be directed to Ascent Research.
