BLVRA Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of HCT 116 colorectal carcinoma cells with targeted disruption of the BLVRA gene. This loss-of-function model enables investigation of BLVRA-dependent processes without clonal isolation, preserving genetic heterogeneity for robust pooled analyses. The polyclonal knockout format is suited for bulk biochemical studies, functional screens, and assays where monoclonal variation is undesirable.
The parental HCT 116 line is a microsatellite instability-high (MSI-H) human colorectal carcinoma epithelial cell line harboring KRAS G13D and CTNNB1 S45F mutations. These genetic alterations drive constitutive MAPK and Wnt/??-catenin signaling, creating a tumorigenic context that depends on adaptive antioxidant and metabolic pathways. This background makes HCT 116 an appropriate host for interrogating the role of BLVRA in cancer cell stress adaptation and signaling.
BLVRA encodes biliverdin reductase A, a bifunctional enzyme that reduces biliverdin to the antioxidant bilirubin and functions as a serine/threonine kinase. Activated by NRF2, heme, oxidative stress, FOXO1, and HIF1A, BLVRA phosphorylates IRS1 to modulate PI3K/AKT and MAPK/ERK1/2 signaling. The bilirubin product scavenges ROS and influences NF-??B activity. Key interacting factors include biliverdin, NADPH, IRS1, and heme oxygenase-1 (HO-1), positioning BLVRA at the interface of heme catabolism, redox homeostasis, and growth-regulatory pathways.
In HCT 116 cells, loss of BLVRA is predicted to impair bilirubin-mediated antioxidant defense and alter IRS1-dependent PI3K/AKT and MAPK pathway activation. The KRAS G13D-driven MAPK activity and CTNNB1 S45F-stabilized ??-catenin signaling may interact with BLVRA??s functions to affect proliferation, survival, and metabolic adaptability under oxidative stress. This knockout model therefore offers a system to dissect how BLVRA integrates redox control with oncogenic signaling in a colorectal carcinoma background with defined genetic drivers.
This polyclonal knockout cell population is suitable for studying oxidative stress responses, the role of bilirubin in cancer, insulin resistance and metabolic reprogramming, and PI3K/AKT or MAPK pathway modulation. Representative assays include Western blotting for BLVRA and phosphorylated targets (AKT, ERK1/2), bilirubin quantification by HPLC, ROS measurements, cell viability and proliferation assays, phospho-AKT ELISA, and xenograft tumor growth experiments. For further information, contact Ascent Research.
