The DPP7 Knockout HCT 116 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for functional genomics studies, featuring targeted disruption of the DPP7 gene in the HCT 116 human colorectal carcinoma line. This heterogeneous pool of cells with DPP7 loss-of-function maintains genetic diversity while avoiding clonal selection biases, making it ideal for pooled screening and bulk population analyses. As a serine exopeptidase, DPP7 mediates N-terminal X-Pro dipeptide cleavage, and its knockout is expected to impair protein catabolism and proline metabolism.
The HCT 116 cell line is a well-characterized model of colorectal adenocarcinoma, harboring activating mutations in KRAS (G13D) and ??-catenin that drive constitutive oncogenic signaling. These cells exhibit robust proliferation, anchorage-independent growth, and intact apoptosis machinery, positioning them as a standard platform for studying tumorigenesis and drug responses. The mutant KRAS background provides a clinically relevant context for investigating metabolic stress, while the ??-catenin mutation enables crosstalk studies with Wnt pathway components.
DPP7, a lysosomal serine protease, hydrolyzes N-terminal X-Pro dipeptides to regulate intracellular proline pools and facilitate protein turnover. In the apoptotic pathway, DPP7 directly interacts with the anti-apoptotic protein Bcl-2, modulating the Bcl-2/Bax balance to inhibit mitochondrial cytochrome c release and subsequent caspase-3 activation. Upstream, DPP7 expression is controlled by the tumor suppressor p53 and hypoxia-inducible factor HIF1A, integrating DNA damage and oxygen-sensing signals. Downstream, its activity influences proline metabolism and neuropeptide processing, linking lysosomal proteolysis to broader cellular survival networks.
In HCT 116 cells retaining functional p53 and sensitive apoptotic signaling, DPP7 knockout is anticipated to heighten susceptibility to apoptosis triggered by nutrient deprivation or chemotherapeutics. Colorectal carcinomas often rewire proline metabolism to sustain biosynthesis and energy production; loss of DPP7 may compromise this metabolic flexibility, reducing colony formation and viability. The polyclonal nature of this knockout model minimizes clonal artifacts, better reflecting tumor heterogeneity and enabling robust population-level analyses of DPP7-dependent survival mechanisms in a KRAS-mutant background.
This product supports diverse applications including functional genomics, apoptosis research, proline metabolism studies, and drug target validation. Researchers can employ genomic DNA sequencing, RT-qPCR, and western blotting to confirm DPP7 disruption, then perform Annexin V/PI staining or caspase-3 activity assays to quantify apoptosis. Cell viability (MTT) and colony formation assays assess proliferative capacity, while proline quantification directly measures metabolic outcomes. These polyclonal knockout cells are also suitable for pooled screening approaches. For further details, please contact Ascent Research.
