The DPP4 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HCT 116 human colorectal carcinoma cell line, featuring disruption of the DPP4 gene encoding dipeptidyl peptidase 4 (CD26). This polyclonal mixture provides a heterogeneous loss-of-function model for studying DPP4 biology without single-cell clonal constraints.
The HCT 116 host is a well-characterized human colorectal carcinoma epithelial cell line with KRAS (G13D) and PIK3CA (H1047R) mutations, MSH2 deficiency causing microsatellite instability, and wild-type p53. This adherent line is extensively employed in colorectal cancer studies of oncogenic signaling, metabolic reprogramming, and DNA repair defects.
DPP4 is a multifunctional transmembrane serine exopeptidase that cleaves N-terminal dipeptides from substrates with proline or alanine at position 2, including incretins GLP-1 and GIP and chemokine SDF-1 (CXCL12). By inactivating incretins, DPP4 regulates glucose homeostasis, while SDF-1 cleavage modulates CXCR4-mediated migration. DPP4 also functions as a T-cell co-stimulatory molecule (CD26) via interaction with ADA and ECM proteins. Its expression is regulated by TNF-??, IFN-??, EGF, NF-??B, AP-1, and HIF-1??, and it signals downstream through cAMP/PKA, MAPK, and ZAP-70 pathways.
In HCT 116 cells, DPP4 contributes to tumor progression by cleaving SDF-1, affecting the SDF-1/CXCR4 axis, and by interacting with integrin-mediated adhesion pathways, thereby influencing migration and invasion. The KRAS and PIK3CA mutations drive MAPK and AKT signaling, providing an opportunity to study cross-talk with DPP4-dependent pathways. The MSH2 deficiency may alter immune cell interactions, making this model useful for exploring DPP4’s role in the tumor microenvironment and inflammation-driven cancer.
These knockout cells are suitable for a variety of assays, including western blotting and RT-qPCR for DPP4, Sanger sequencing for knockout validation, GLP-1 degradation assays, migration and invasion assays, proliferation, colony formation, phospho-signaling (ERK, AKT), and apoptosis (caspase-3/7). The product supports colorectal cancer research, DPP4 inhibitor screening, incretin signaling studies, cancer metabolism analysis, and tumor-immune microenvironment investigations. For additional details, please contact Ascent Research.
