The ATG16L1 Knockout Ca Ski Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal population of Ca Ski cells with disrupted ATG16L1, generating a loss-of-function model. It is designed to study ATG16L1-dependent autophagy and immune signaling in a cervical carcinoma background. The polyclonal format preserves tumor heterogeneity and is supplied ready-to-use for downstream experiments.
Ca Ski cells, an HPV-16-positive cervical epithelial carcinoma line, serve as a model for HPV-driven cancers. The viral oncoproteins E6 and E7 inactivate p53 and Rb, fostering immortalization and enabling studies of virus-host autophagy interactions. This line is widely used for cervical cancer research on drug resistance, invasion, and immune evasion.
ATG16L1 serves as a scaffold in the ATG12?CATG5-ATG16L1 complex, directing LC3 and GABARAP lipidation to phagophore membranes for autophagosome biogenesis. It functions downstream of mTOR, AMPK, and ULK1, and is transcriptionally regulated by TFEB and FOXO3. ATG16L1 directly binds ATG5 and ATG12, recruiting WIPI2 and RB1CC1/FIP200 to autophagosome formation sites. Beyond autophagy, ATG16L1 suppresses NF-??B activation and RIG-I/MAVS-mediated type I interferon production, and is regulated by TNF?? and IFN??. Disruption of ATG16L1 leads to impaired LC3 lipidation, p62/SQSTM1 accumulation, and dysregulated pro-inflammatory signaling.
In Ca Ski cells, ATG16L1 knockout provides a powerful system to dissect autophagy’s role in HPV-driven oncogenesis and therapeutic response. ATG16L1-dependent autophagy often promotes tumor cell survival under metabolic stress and contributes to drug resistance. This model enables investigation of how HPV oncoproteins intersect with ATG16L1 to regulate NF-??B signaling and immune evasion, and is valuable for assessing autophagy deficiency effects on cervical cancer progression, apoptosis sensitivity, and response to chemotherapeutic agents or immunotherapy.
Applications include Western blotting for LC3-II and p62 to monitor autophagic flux, fluorescence microscopy for LC3 puncta, and flux assays with bafilomycin A1. Flow cytometry assesses apoptosis, while co-immunoprecipitation probes ATG16L1 interactions with ATG5 and ATG12, and NF-??B reporter assays evaluate inflammatory signaling. The model supports studies on HPV-mediated immune evasion, drug resistance, and autophagy’s role in diseases like Crohn??s disease. For further information, please contact Ascent Research.
