In Stock Cell Lines
Homo sapiens (Human)
Large intestine (colon)
Adherent
The DCC Knockout SW480 Cell Line is a CRISPR/Cas9-edited colorectal adenocarcinoma model with targeted disruption of the DCC tumor suppressor gene. Derived from SW480 cells harboring APC, KRAS, and TP53 mutations, this line enables study of DCC??s role as a netrin-1 dependence receptor, which governs caspase-9/?3-mediated apoptosis in the absence of ligand and promotes AKT/ERK survival signaling upon NTN1 binding. Loss of DCC abrogates this apoptotic brake, mirroring epigenetic silencing in colorectal cancer. Applications include apoptosis assays, migration studies, co?immunoprecipitation with UNC5 receptors, drug screening, and xenograft models to dissect dependence receptor signaling and tumor progression.
The DCC Knockout SW480 Cell Line is a CRISPR/Cas9-edited human colorectal adenocarcinoma cell product in which the DCC gene has been disrupted to create a loss-of-function model. This knockout cell line enables investigation of DCC-dependent signaling mechanisms in a well-characterized intestinal epithelial background.
The parental SW480 cell line was originally established from a Dukes’ type B colorectal adenocarcinoma and is widely employed in colorectal cancer research. SW480 cells carry oncogenic mutations in APC, KRAS, and TP53, rendering them a robust platform for studying genetic interactions and tumor suppressor pathways in a disease-relevant context.
DCC encodes a transmembrane dependence receptor for the guidance cue netrin-1 (NTN1). In the presence of NTN1, DCC activates downstream survival and migratory signaling through PI3K/AKT and MAPK/ERK pathways, engaging effectors such as AKT, ERK1/2, FAK, and Rho GTPases including RhoA and Rac1. Unliganded DCC, however, triggers apoptosis by recruiting and activating caspase-9, which subsequently processes caspase-3. DCC also heterodimerizes with UNC5 family receptors (UNC5A?CD) to modulate divergent signaling outcomes, and interacts with adaptor proteins such as DIP13??/APPL1. Epigenetic silencing of DCC, frequently mediated by promoter methylation and DNA methyltransferases, constitutes a known mechanism of tumor suppressor inactivation in colorectal cancers.
In the SW480 background, which already harbors defects in APC, KRAS, and TP53, disruption of DCC eliminates its pro-apoptotic dependence receptor function, mimicking the epigenetic silencing observed in advanced colorectal tumors. This knockout thus provides a physiologically relevant system to dissect how loss of netrin-1/DCC-mediated apoptotic signaling cooperates with other oncogenic alterations to promote tumor progression, chemoresistance, and metastatic behavior.
Researchers can employ this cell line in a variety of functional assays, including Western blotting and RT-qPCR to confirm DCC ablation and monitor caspase-3, caspase-9, or AKT/ERK phosphorylation status; Annexin V/propidium iodide apoptosis assays; Transwell migration and invasion studies; co-immunoprecipitation of DCC with NTN1 or UNC5 receptors; immunofluorescence; and xenograft tumor growth models. Additional applications include drug screening for netrin-1 pathway modulators and epigenetic reactivation studies using DNA methylation inhibitors. For additional details or custom project inquiries, please contact Ascent Research.
