CD36 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the Ca Ski human cervical carcinoma line, engineered to disrupt the CD36 gene. This heterogeneous pool enables loss-of-function studies without clonal selection bias, preserving population-level diversity for functional interrogation of CD36-dependent pathways. The polyclonal format is suitable for pooled knockout experiments or subsequent clonal isolation, providing a stable, heritable disruption for reproducible in vitro investigations.
Ca Ski is a widely used human epithelial cervical cancer cell line, originally established from a metastatic site of squamous cell carcinoma. It harbors integrated HPV-16 genomes, making it a relevant model for HPV-driven oncogenesis. Ca Ski cells retain typical epithelial features and are applied in studies of cervical cancer biology, tumor microenvironment interactions, and drug testing. Combining CD36 disruption with this background allows dissection of lipid and inflammatory pathways specifically in HPV-positive cervical carcinoma.
CD36 is a scavenger receptor and fatty acid translocase that mediates uptake of long-chain fatty acids, oxidized LDL (oxLDL), and thrombospondin-1 (THBS1). Transcriptionally regulated by PPARG, NR1H3, and SREBF1, its signaling activates Fyn and Lyn kinases, leading to MAPK (ERK, JNK, p38) and NF-??B pathways, and promotes expression of COX-2, VEGF, and matrix metalloproteinases. CD36 forms complexes with TLR4/TLR6 heterodimers and integrins ??1/??3, cooperating with Caveolin-1 and FABP4 for lipid trafficking. Fatty acid import fuels CPT1-dependent mitochondrial ??-oxidation, while THBS1 binding triggers TGF-?? activation, connecting CD36 to angiogenesis control and innate immunity.
In Ca Ski cells, CD36 disruption likely impairs lipid uptake and metabolic reprogramming, critical for cervical cancer proliferation. Loss of fatty acid-driven ??-oxidation may sensitize cells to metabolic stress. Abrogation of CD36?CTHBS1 signaling could alter TGF-?? activation, impacting angiogenesis and migration. In the HPV-16 context, CD36 knockout may reshape TLR4/NF-??B-mediated inflammatory networks, offering a model to dissect metabolic-immune crosstalk in cervical carcinoma and identify therapeutic targets.
Applications include BODIPY-based fatty acid uptake and fluorescent oxLDL uptake assays, coupled with Seahorse metabolic flux analysis to evaluate ??-oxidation. THBS1/CD36 interaction can be probed via co-immunoprecipitation and Western blot for phospho-ERK or NF-??B. Scratch wound assays assess migration, while RT-qPCR arrays screen lipid metabolism genes. Flow cytometry confirms CD36 surface loss. These cells enable studies on metabolic reprogramming, thrombospondin-1 signaling, and therapeutic resistance in cervical cancer. Contact Ascent Research for further details.
