The APP Knockout DLD-1 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the DLD-1 human colorectal adenocarcinoma cell line. Engineered via CRISPR/Cas9-mediated target-gene disruption, this model provides a genetically defined loss-of-function system for investigating the role of the amyloid precursor protein (APP) in epithelial cell biology and disease. The polyclonal pool retains genetic heterogeneity, enabling robust population-level analysis without clonal artifacts.
DLD-1 is a well-characterized human colorectal adenocarcinoma cell line with epithelial morphology, originally established from a primary tumor of the colon. It serves as a widely utilized in vitro model for studying colorectal cancer pathogenesis, including cell adhesion, migration, proliferation, and signal transduction. The DLD-1 genetic background harbors mutations commonly associated with colorectal tumorigenesis, such as in APC and KRAS, making it a relevant platform for dissecting oncogenic signaling networks and evaluating potential therapeutic targets.
APP gene encodes a type I transmembrane protein that undergoes sequential proteolytic processing by ??- and ??-secretase complexes, generating amyloid-?? (A??) peptides and the APP intracellular domain (AICD). In epithelial cancer models, APP modulates cell adhesion, migration, and proliferation through downstream AKT and ERK pathways. AICD translocates to the nucleus and, with APBB1 (Fe65) and Tip60, regulates transcription. APP is cleaved by BACE1 and the ??-secretase complex (PSEN1, PSEN2, NCSTN, APH1A, PEN2), and its function is influenced by upstream regulators such as EGF/EGFR, NOTCH1, and transcription factors SP1, REST, CTCF. Downstream, APP impacts GSK3B, p53, BAX, and NEP, linking it to neurodegenerative and oncogenic pathways.
In the context of colorectal adenocarcinoma, aberrant APP expression and processing have been implicated in tumor progression, metastasis, and resistance to apoptosis. By disrupting APP in DLD-1 cells, this knockout population enables interrogation of APP-dependent mechanisms in epithelial tumor biology. The model is particularly suited for dissecting APP-mediated crosstalk with PI3K/AKT, Wnt, and Notch pathways, all of which are frequently dysregulated in colorectal cancer. Loss of APP function can unveil alterations in cell adhesion dynamics, invasive capacity, and proliferative control, providing insights into the protein’s contribution to oncogenic phenotypes.
Researchers can employ this polyclonal knockout cell population in Western blotting and RT-qPCR for APP loss verification, phenotypic assays such as migration, invasion, and cell adhesion to assess metastatic traits, and amyloid-?? ELISA or phospho-AKT/ERK analysis for signaling readouts. Co-immunoprecipitation can map partners like APBB1, APLP1/2, or ??-secretase components. These cells are also valuable for high-throughput screening of APP modulators and as isogenic controls in drug sensitivity assays. For further information, please contact Ascent Research.
