The CD38 Knockout DLD-1 Polyclonal Cells represent a CRISPR/Cas9-mediated gene-disrupted cell population derived from the DLD-1 human colorectal adenocarcinoma cell line. This polyclonal knockout model provides a heterogeneous loss-of-function background for studying CD38-dependent signaling, metabolism, and cellular functions. The polyclonal nature ensures genetic diversity, enabling robust assessment of gene function in a population context, while minimizing clonal artifacts. This product serves as a versatile tool for elucidating the roles of CD38 in cancer biology, immunoregulation, and extracellular nucleotide metabolism.
DLD-1 is a well-characterized adherent epithelial line established from a Duke’s type C colorectal adenocarcinoma and harbors mutations in APC, TP53, and KRAS, which are cardinal genetic alterations in colorectal carcinogenesis. The cell line retains epithelial morphology and exhibits anchorage-independent growth, making it a standard model for examining oncogenic signaling, tumor microenvironment interactions, and therapeutic responses. Its genetic background reflects key pathways dysregulated in colorectal cancer, providing a clinically relevant cellular system for functional genomics studies.
CD38 is a multifunctional ectoenzyme with ADP-ribosyl cyclase and NAD+ glycohydrolase activities, catalyzing the synthesis of cyclic ADP-ribose (cADPR) and ADP-ribose (ADPR) from NAD+. cADPR mobilizes intracellular Ca2+ via ryanodine receptors and TRPM2 channels, while ADPR modulates Ca2+-dependent kinases. CD38 also acts as a receptor for CD31, triggering MAPK/ERK, NF-??B, and PI3K/Akt signaling cascades. Its NADase activity regulates NAD+ bioavailability, impacting sirtuin-1 (SIRT1) and cellular metabolism. CD38 expression is induced by TNF-??, IL-1??, and IFN-??, and it interacts with molecules such as CD19, ZAP-70, and caveolin-1, positioning CD38 at the nexus of extracellular nucleotide signaling and intracellular calcium and metabolic networks.
In the DLD-1 colorectal cancer context, CD38-mediated calcium signaling and NAD+ metabolism intersect with pathways commonly altered by APC, TP53, and KRAS mutations. The knockout model enables dissection of how CD38 influences NF-??B and MAPK/ERK signaling, thereby contributing to malignant phenotypes such as proliferation, survival, migration, and immune evasion. By eliminating CD38 expression, researchers can probe its role in modulating tumor-intrinsic signaling and the response to microenvironmental cues, offering insights into mechanisms of colorectal cancer progression and potential therapeutic vulnerabilities.
This knockout product supports applications including calcium imaging to study CD38-driven calcium dynamics, NAD+/NADH quantification for metabolic profiling, and phospho-signaling analysis by western blotting. It enables drug sensitivity assays for anti-CD38 resistance, migration/invasion studies, and co-immunoprecipitation to map protein interactions. Transcriptomic approaches such as RNA-seq can uncover global gene expression changes. For detailed technical specifications, validation data, or ordering inquiries, please contact Ascent Research.
