The CD36 Knockout 143B Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 143B human osteosarcoma cell line. This product provides a loss-of-function model for studying CD36-mediated signaling and metabolic processes. Through CRISPR/Cas9-mediated gene disruption, the CD36 locus is targeted to ablate functional receptor expression across a heterogeneous cell pool, enabling researchers to examine CD36-dependent phenotypes without clonal artifacts.
The 143B cell line is a well-characterized model of human osteosarcoma, originating from a bone tumor and widely employed in cancer research to investigate tumor growth, invasion, and metastasis. Its aggressive nature and defined genetic background make it particularly suitable for dissecting pathways that control cancer progression and metabolic adaptation. 143B cells retain key features of osteosarcoma, including high metastatic potential, providing a physiologically relevant context for knockout studies.
CD36 is a multifunctional scavenger receptor that binds diverse ligands, including thrombospondin-1 (TSP-1), oxidized low-density lipoprotein (OxLDL), and long-chain fatty acids. Ligand engagement triggers intracellular cascades through interactions with integrin ??1, integrin ??5, TLR4, TLR6, and tetraspanins such as CD9 and CD81. Upstream transcription factors PPAR??, CEBP??, and NF-??B regulate CD36 expression, while downstream effectors include Src family kinases, MAPK, FAK, and JNK. Representative signaling modules??TSP-1/CD36/Src/MAPK and OxLDL/CD36/NF-??B??mediate processes like angiogenesis, inflammatory responses, and lipid internalization. In the 143B background, disrupting CD36 decouples these pathways from receptor input, revealing their contributions to cellular behavior.
In osteosarcoma, CD36 has been implicated in metastatic propensity and metabolic reprogramming, particularly through fatty acid uptake and utilization. The polyclonal knockout population enables bulk analysis of CD36 loss in a setting that mirrors the genetic variability of tumors, avoiding biases introduced by monoclonal selections. Researchers can interrogate how CD36 ablation affects tumor cell migration, invasion, and response to metabolic stress, providing insights into CD36 as a potential vulnerability in osteosarcoma and other lipid-dependent cancers.
This knockout product is suited for a range of functional assays, including fatty acid uptake measurements, Boyden chamber migration/invasion assays, and Western blotting for phospho-Src and MAPK to assess signaling outputs. Flow cytometry confirms loss of CD36 surface expression, while qRT-PCR monitors downstream target genes. Additional applications encompass apoptosis assays and drug sensitivity testing to evaluate therapeutic strategies targeting lipid metabolism. By employing these analytical approaches, researchers can dissect CD36??s role in oncogenic signaling and metabolic adaptation. For further technical details, please contact Ascent Research.
