KDR 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 targeted disruption of the KDR gene (VEGFR2). This product provides a genetically diverse pool of cells with KDR loss-of-function, enabling robust phenotypic analyses without clonal artifacts.
HCT 116 is an epithelial cell line widely used as a model for colorectal adenocarcinoma. It carries an activating KRAS G13D mutation and exhibits high microsatellite instability due to MLH1 deficiency. These characteristics are relevant for studying signal transduction and therapeutic resistance in colorectal cancer. The adherent cells maintain epithelial morphology, offering a well-characterized platform for knockout-based investigations.
KDR encodes VEGFR2, which binds VEGF-A, VEGF-C, and VEGF-D. Ligand engagement triggers receptor dimerization and autophosphorylation, recruiting adaptor proteins such as Grb2 and Shc. This activates downstream effectors including PI3K-Akt, PLC??-PKC, and MAPK/ERK cascades, as well as FAK and Src. KDR signaling promotes endothelial cell survival, proliferation, migration, and vascular permeability. Coreceptors Neuropilin-1 and integrin ??v??3 enhance signaling, while HIF-1?? upregulates KDR under hypoxia. Key downstream targets include mTOR, eNOS, and pro-survival gene expression programs.
In HCT 116 cells, KDR knockout enables dissection of autocrine VEGF signaling pathways that may influence tumor cell migration, invasion, and survival. Crosstalk between oncogenic KRAS and VEGFR2 could modulate tumor aggressiveness and response to anti-angiogenic drugs. The MSI-high background also supports studies on how VEGF signaling affects the tumor immune microenvironment. This polyclonal knockout tool is therefore valuable for translational research in colorectal cancer.
Researchers can employ this knockout model for Western blot analysis of phospho-KDR and downstream signaling proteins (Akt, ERK, FAK), RT-qPCR profiling of VEGF-responsive genes, migration and invasion assays, and drug sensitivity tests with sunitinib or bevacizumab. Immunofluorescence or flow cytometry verifies KDR loss, while co-culture with endothelial cells assesses paracrine angiogenesis. For custom inquiries or additional services, please contact Ascent Research.
