In Stock Cell Lines
Homo sapiens (Human)
Large intestine (colon)
Adherent
The DCC Knockout SW620 Cell Line is a CRISPR/Cas9-edited human colorectal adenocarcinoma cell line with targeted disruption of the DCC gene, which encodes the netrin-1 dependence receptor. Derived from the metastatic SW620 line, this model reflects DCC loss in colorectal cancer, where DCC normally functions as a tumor suppressor by promoting apoptosis and limiting cell migration. DCC signaling involves netrin-1 ligand binding, UNC5 co-receptors, and downstream pathways such as MAPK/ERK, PI3K/AKT, and Rho GTPases, including RAC1. This knockout cell line is ideal for studying apoptosis, migration, invasion, and therapeutic resistance in colorectal cancer research, utilizing assays such as Western blotting, Transwell migration, and Annexin V apoptosis assays.
PAM Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG16748
HSDL2 Knockout jurkat Polyclonal Cells
Cat. No. ARG34284
CAPN1 Knockout Hela Polyclonal Cells
Cat. No. ARG42162
CALM3 Knockout HAP1 Polyclonal Cells
Cat. No. ARG41873
CDKL5 Knockout HCT116 Polyclonal Cells
Cat. No. ARG7308
NUB1 Knockout AGS Polyclonal Cells
Cat. No. ARG3218
The DCC Knockout SW620 Cell Line is a CRISPR/Cas9-edited human knockout cell line based on the SW620 colorectal adenocarcinoma epithelial line. This model features DCC gene disruption, encoding the netrin-1 dependence receptor with critical roles in apoptosis, cell migration, and tumor suppression. It provides a robust loss-of-function system for studying DCC-dependent signaling pathways in colorectal cancer. CRISPR/Cas9-mediated gene disruption enables precise interrogation of DCC function without partial silencing artifacts.
The SW620 cell line was derived from a lymph node metastasis of a Dukes’ type C colorectal adenocarcinoma from a male patient. This highly tumorigenic and metastatic model retains key features of advanced colorectal cancer, including invasive potential and aberrant signaling. This background makes the DCC knockout particularly relevant for studying progression to metastatic dissemination. SW620 is widely used in metastasis assays, drug resistance studies, and tumor microenvironment research.
DCC functions as a transmembrane dependence receptor for netrin-1; in the absence of ligand, it promotes apoptosis through caspase-9 and caspase-3 activation. Upon netrin-1 binding, DCC activates cell survival and migration signaling via MAPK1/3 (ERK1/2) and PI3K/AKT pathways, while also regulating Rho GTPases such as RAC1 and RHOA. DCC interacts with UNC5 co-receptors (UNC5A/UNC5B) to modulate netrin sensitivity and signaling outcomes. Upstream, DCC is regulated by p53 transcriptional activity, caspase-mediated cleavage, and epigenetic silencing; downstream, it influences pro-apoptotic factors BAX and PUMA, as well as MYC expression. This intricate network positions DCC as a molecular switch between cell death and survival/guidance responses.
In colorectal cancer, DCC is frequently lost or silenced, disrupting tumor suppression. The DCC Knockout SW620 Cell Line recapitulates this loss in a metastatic background, enabling dissection of how DCC deficiency enhances cell survival, migration, and invasion. It is useful for studying netrin-1-dependent and -independent effects on tumor progression and for evaluating therapeutic strategies targeting DCC restoration or downstream pathways. Comparing wild-type and knockout cells identifies critical signaling nodes driving metastasis.
This cell line is suited for diverse applications, including Western blotting and RT-qPCR to confirm DCC disruption and assess downstream signaling; Transwell migration and invasion assays to evaluate metastatic behavior; apoptosis assays using Annexin V and flow cytometry; co-immunoprecipitation to probe protein interactions; and cell viability assays for drug sensitivity testing. It provides a powerful tool for studying DCC roles in netrin biology, tumor suppression, and therapeutic resistance. For further information or technical support, contact Ascent Research.
