The CD36 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the CD36 gene in the human oral squamous cell carcinoma (OSCC) cell line CAL-27. This heterogeneous pool minimizes clonal selection artifacts, offering a robust model for studying CD36 deficiency in population-level phenotypes such as metabolic reprogramming and drug response.
CAL-27, derived from a human tongue squamous cell carcinoma, is a widely used adherent cell line that retains epithelial characteristics and tumorigenic capacity. It is commonly applied to study oral cancer proliferation, invasion, and chemoresistance. Disrupting CD36 in this background allows dissection of lipid-regulated pathways in a disease-relevant context.
CD36 is a scavenger receptor that mediates uptake of long-chain fatty acids and oxidized LDL. Upon ligand binding, it recruits Src family kinases Fyn and Lyn, leading to JNK and NF-??B activation and inflammatory cytokine transcription. CD36 also complexes with thrombospondin-1, integrins (??V??3, ??6??4), TLR2/4, caveolin-1, and tetraspanins CD9/CD81. Upstream, its expression is induced by PPAR?? agonists, fatty acids, and HIF-1??; downstream, it drives PPAR?? activation and CPT1A-mediated fatty acid oxidation. Thus, CD36 integrates lipid sensing with MAPK, NF-??B, and TGF-?? pathways.
In oral squamous cell carcinoma, CD36 promotes tumor progression by supplying fatty acids for energy and anabolism, and by activating oncogenic signaling. Its knockout is expected to impair lipid uptake, sensitize cells to metabolic stress, and reduce NF-??B- and TGF-??-driven proliferation and migration. This model is thus valuable for studying metabolic vulnerabilities and drug resistance in OSCC.
Researchers can employ this polyclonal knockout pool in fatty acid uptake and oil red O staining assays to assess lipid handling, and Seahorse analysis to measure metabolic flux. Western blotting for phosphorylated JNK, NF-??B, and Fyn can reveal signaling alterations, while RT-qPCR quantifies metabolic gene expression (e.g., CPT1A, PPAR??). Phenotypic assays include MTT/BrdU proliferation, scratch wound/transwell migration, and Annexin V apoptosis. The cells are also suitable for RNA-seq, immunoprecipitation of CD36 interactors, and in vivo xenograft growth studies. For further information and detailed protocols, please contact Ascent Research.
