The CD36 Knockout DLD-1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population derived from the DLD-1 human colorectal adenocarcinoma cell line, in which the CD36 gene has been disrupted to generate a loss-of-function model. This polyclonal knockout product provides a heterogeneous pool of CD36-deficient cells suitable for studying CD36-dependent processes in colorectal cancer biology. The CRISPR/Cas9-mediated gene disruption eliminates CD36 protein expression across the population, enabling robust investigation of CD36 function without the clonal selection artifacts often associated with single-cell-derived knockouts.
The parental DLD-1 cell line was established from a primary colorectal adenocarcinoma of a male patient with Dukes’ type C disease. These epithelial cells are widely used as an in vitro model for colorectal cancer progression, intestinal epithelial barrier integrity, and metastatic behavior. DLD-1 cells retain key oncogenic and tumor-suppressor pathway alterations typical of colorectal tumors, making them a relevant system for dissecting molecular mechanisms underlying colorectal pathogenesis and therapeutic resistance.
CD36 encodes a multifunctional scavenger receptor that mediates the cellular uptake of long-chain fatty acids and oxidized low-density lipoprotein (oxLDL). CD36 is transcriptionally regulated by PPAR??, Nrf2, LXR, PXR, IL-4/STAT6 signaling and acts upstream of downstream effectors including NF-??B, JNK, p38 MAPK, Src kinases, and caspase-3. It interacts with ligands such as thrombospondin-1, integrin ??v??3, and co-receptors TLR2/TLR6, as well as kinases Lyn and Fyn. These interactions integrate CD36 into pathways controlling lipid droplet formation, inflammatory responses, and apoptotic clearance. In the context of colorectal cancer, CD36-mediated fatty acid import fuels mitochondrial ??-oxidation and anabolic metabolism, while oxLDL engagement can trigger pro-inflammatory signaling cascades.
Disruption of CD36 in DLD-1 cells allows researchers to probe the receptor’s role in tumor-specific lipid handling and energy metabolism. Given DLD-1’s origin and widespread use in cancer biology, this knockout model is particularly valuable for examining how CD36 contributes to fatty acid uptake-driven proliferation, angiogenesis, and survival under metabolic stress. Furthermore, CD36 signaling through thrombospondin-1 modulates TGF-?? activation and extracellular matrix remodeling, processes critical for tumor invasion and metastasis. The polyclonal nature of the knockout preserves the heterogeneity of the original tumor cell population, facilitating realistic studies of phenotypic variability and drug response.
Typical applications include investigating the contribution of CD36 to fatty acid metabolism and lipid signaling using BODIPY-labeled fatty acid uptake and oil red O staining for neutral lipid accumulation. Researchers can also employ immunofluorescence and western blotting to confirm CD36 loss, RT-qPCR to assess transcriptional changes, and wound healing or proliferation assays to evaluate metastatic and growth phenotypes. Flow cytometry for apoptosis markers and oxLDL uptake assays further enable dissection of CD36’s role in programmed cell death and scavenger function. These applications support drug resistance studies related to lipid uptake and the development of CD36-targeted therapeutic strategies. For further information, please contact Ascent Research.
