The CD36 Knockout A2780 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma cell line. The cells harbor a targeted disruption of the CD36 gene, generated by CRISPR/Cas9 genome editing without selection of a clonal isolate. This polyclonal knockout model provides a heterogeneous pool of gene-edited cells for functional studies of CD36 in a disease-relevant background. The loss-of-function system enables investigation of CD36-mediated processes in ovarian cancer biology, lipid metabolism, and therapeutic response without the limitations of single-clone artifacts.
The A2780 cell line was originally established from an untreated patient with ovarian carcinoma and displays epithelial morphology. These cells are well-characterized as a cisplatin-sensitive epithelial ovarian cancer model, widely employed in chemoresistance and metastasis research. The parental A2780 line retains key molecular features of the disease, making it a suitable host for gene perturbation studies aimed at dissecting pathways that drive ovarian cancer progression and drug sensitivity.
CD36 encodes a multifunctional scavenger receptor that binds oxidized low-density lipoprotein, long-chain fatty acids, and thrombospondin-1 (THBS1). Through these interactions, it mediates lipid uptake and cellular adhesion while activating intracellular signaling networks. Upstream transcription factors including PPARG, NFKB1, TGFB1, HIF1A, and LXR regulate CD36 expression. Upon ligand engagement, CD36 stimulates SRC and MAPK1/3 kinases, leading to NFKB1 activation and upregulation of fatty acid oxidation genes like CPT1A. The receptor physically interacts with THBS1, LYN, ITGB1, and SRC, forming signaling platforms that promote the CD36/THBS1/FYN/p38MAPK cascade and the CD36/oxLDL/NFKB pathway. In metabolic contexts, CD36-driven fatty acid import activates PPAR signaling, linking nutrient uptake to transcriptional control.
In ovarian cancer, CD36 has emerged as a critical mediator of metastasis and chemoresistance, partly through its role in promoting fatty acid oxidation. The A2780 knockout model, being cisplatin-sensitive, offers a unique tool to dissect how CD36-dependent lipid metabolism contributes to the acquisition of drug resistance. By comparing edited and parental cells, researchers can examine the impact of CD36 loss on tumor cell behavior, including migration, invasion, and survival under therapeutic stress. This model is particularly valuable for exploring the intersection of metabolic reprogramming and oncogenic signaling in epithelial ovarian carcinoma.
Typical applications include investigating the mechanisms by which CD36 supports ovarian cancer metastasis and cisplatin resistance, screening novel CD36-targeted compounds, and assessing the receptor??s role in lipid uptake and storage. Researchers can employ a panel of validated assays with these cells, such as western blotting and RT-qPCR to confirm target disruption and pathway changes, fatty acid uptake assays and Oil Red O staining to monitor lipid accumulation, flow cytometry for surface CD36 expression, migration and invasion assays to evaluate metastatic potential, and drug sensitivity tests to quantify cisplatin response. For technical product inquiries, please contact Ascent Research.
