The ATG7 Knockout CAL-27 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from the CAL-27 human oral squamous cell carcinoma line, engineered for loss-of-function studies of the ATG7 gene. This polyclonal population enables investigation of ATG7-dependent pathways without clonal selection artifacts. Gene disruption abrogates ATG7 function, allowing assessment of its role in autophagy and cancer-relevant processes.
CAL-27 is an epithelial cell line originally from a 56-year-old male with tongue squamous cell carcinoma, widely used as an oral cancer model. It retains key tumorigenic characteristics and is reliable for studying cancer signaling, drug response, and metastasis.
ATG7 encodes an E1-like enzyme that catalyzes two ubiquitin-like conjugation systems in autophagy: ATG12 conjugation to ATG5 and LC3 lipidation. ATG7 activates ATG12 for transfer to ATG5, forming the ATG12?CATG5?CATG16L1 complex, and activates LC3 for membrane conjugation. ATG7 acts downstream of mTORC1 and AMPK, and upstream of LC3-II formation and p62 degradation. Transcriptional regulation by TFEB and FOXO3 links ATG7 to stress responses. Through interactions with ATG3, ATG12, and LC3 family members such as MAP1LC3B, ATG7 orchestrates autophagosome biogenesis and mitochondrial quality control.
In CAL-27 cells, ATG7 knockout eliminates autophagic flux, impairing degradation of damaged organelles and aggregated proteins, and increasing susceptibility to microenvironmental stresses such as nutrient deprivation and hypoxia. This model is instrumental for dissecting autophagy??s context-dependent roles in tumor suppression versus tumor promotion, especially in oral squamous cell carcinoma progression, metabolic adaptation, and drug resistance.
Typical applications encompass Western blot analysis of LC3-I/II conversion and p62/SQSTM1 accumulation, fluorescence microscopy of GFP-LC3 puncta, and autophagy flux assays using bafilomycin A1. Additional functional assays include cell viability under nutrient deprivation, wound healing, transwell invasion, and chemotherapeutic sensitivity profiling to identify autophagy-dependent pathways. This product is well-suited for research in cancer biology, autophagy mechanisms, cell death regulation, and oral cancer progression. For custom experimental designs or technical support, please contact Ascent Research.
