The CD38 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population originating from the A2780 human ovarian carcinoma cell line, featuring targeted disruption of the CD38 gene. This loss-of-function model enables systematic investigation of CD38??s multifaceted roles in NAD+ metabolism, calcium signaling, and tumor microenvironment interactions. The polyclonal format preserves genetic diversity, minimizing clonal biases and better representing the heterogeneous editing outcomes typical of CRISPR/Cas9-mediated gene disruption.
The A2780 cell line was established from an untreated patient with epithelial ovarian carcinoma and is widely employed as a model for high-grade serous ovarian cancer. These adherent epithelial cells retain key oncogenic features, including aberrant proliferation, adhesion, and signaling pathways. Their well-characterized chemosensitivity and extensive use in cancer biology make A2780 an appropriate host for studying CD38 in the context of ovarian carcinoma.
CD38 encodes a multifunctional ectoenzyme that catalyzes the synthesis of cyclic ADP-ribose (cADPR) and ADP-ribose from NAD+. cADPR serves as a second messenger, binding to ryanodine receptors (RyRs) on the endoplasmic reticulum to promote calcium release into the cytosol, thereby modulating calcium-dependent processes. Downstream, CD38 activity influences AMPK, SIRT1, and mTOR, integrating NAD+ availability with cellular energy homeostasis and survival. Additionally, CD38 acts as an adhesion receptor for CD31 (PECAM-1), facilitating cell-cell contacts and bidirectional signaling. Upstream regulators include all-trans retinoic acid, 1,25-dihydroxyvitamin D3, interferon-gamma, NF-??B, and IL-2, while its ectoenzymatic activity directly impacts NAD+ and cADPR levels. In immune cells, CD38 associates with the BCR complex, SLP-76, and Lck, though in epithelial cells its primary functions relate to nucleotide metabolism and adhesion.
In A2780 ovarian carcinoma cells, CD38 contributes to tumor progression by modulating extracellular nucleotide pools, promoting CD31-mediated adhesion, and potentially dampening antitumor immune responses. The polyclonal CD38 knockout model permits dissection of how CD38 loss affects intracellular calcium oscillations, NAD+ consumption, and interactions with the tumor microenvironment. This system is valuable for studying epithelial ovarian cancer mechanisms where CD38-driven signaling may enhance proliferation, migration, or chemoresistance.
This knockout product supports a wide range of experimental applications. Researchers can perform flow cytometry to verify CD38 ablation, western blotting, quantitative NAD+/NADH measurements, and fluorometric calcium flux assays to interrogate cADPR-dependent calcium mobilization. It is particularly useful for drug sensitivity testing with anti-CD38 monoclonal antibodies such as daratumumab, alone or in combination with standard chemotherapeutics, using cell viability and apoptosis assays. Additional applications include studies of NAD+ metabolism, immune evasion mechanisms, and therapeutic development for diseases like multiple myeloma and chronic lymphocytic leukemia. For more information or customized products, please contact Ascent Research.
