The CD36 Knockout 769-P Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human 769-P renal cell carcinoma line. This product provides a heterogeneous pool of cells with disruption of the CD36 gene, enabling loss-of-function studies without clonal selection. The polyclonal format preserves genetic diversity while ensuring that the majority of cells harbor targeted gene disruption, making it suitable for population-level phenotypic analyses.
The 769-P cell line is an established model of clear cell renal cell carcinoma (ccRCC), a subtype characterized by aberrant lipid accumulation and metabolic reprogramming. Originally isolated from a primary renal adenocarcinoma, 769-P cells retain key features of ccRCC, including constitutive hypoxia-inducible factor activation and altered lipid metabolism, providing a physiologically relevant context for investigating tumor-associated pathways.
CD36 encodes a transmembrane scavenger receptor that functions as a fatty acid translocase, mediating the uptake of long-chain fatty acids and oxidized LDL. It also binds thrombospondin-1 and collaborates with ??1 and ??5 integrins, CD9, and CD81 to modulate adhesive and signaling functions. CD36 expression is regulated by PPAR?? and NF-??B, and its downstream signaling involves activation of Src family kinases, the MAPK pathway, and NF-??B, ultimately promoting lipid droplet formation and inflammatory responses. Through its interaction with TLR4/TLR6 and MyD88, CD36 also contributes to innate immune signaling. Representative pathway components include FABP4, ACSL1, and DGAT.
In the context of ccRCC, CD36-mediated lipid uptake may fuel tumor growth and metastasis by providing energy substrates and generating signaling lipids. Knockout of CD36 in 769-P cells is expected to impair fatty acid uptake, reduce lipid droplet accumulation, and attenuate pro-inflammatory and pro-metastatic signaling pathways. This model thus allows dissection of how metabolic inputs controlled by CD36 intersect with oncogenic signaling networks in renal cell carcinoma.
These polyclonal knockout cells are ideal for investigating CD36??s role in lipid metabolism, metabolic reprogramming, and cancer progression. They support a range of assays including western blotting for CD36 loss, fatty acid uptake assays, cell proliferation and migration assays, and lipid droplet staining. Downstream pathway interrogation can be performed via RT-qPCR for targets such as FABP4 and ACSL1. The model is also suitable for drug screening studies targeting CD36-mediated processes. For further details or to request custom knockout models, please contact Ascent Research.
