The IQGAP2 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population with IQGAP2 gene disruption in HT29 colorectal adenocarcinoma cells. This loss-of-function model enables study of the scaffold protein IQGAP2, a tumor suppressor regulating actin dynamics, cell adhesion, and signaling. The polyclonal format preserves genetic heterogeneity, offering a realistic system for investigating IQGAP2-dependent mechanisms in colorectal cancer. The product is supplied as a cryopreserved stock ready for expansion and experimentation.
HT29 is a human colorectal adenocarcinoma cell line derived from a 44-year-old female tumor. These epithelial cells form polarized monolayers, produce mucins, and can undergo differentiation, making them a key model for intestinal biology and cancer research. HT29 cells express E-cadherin and exhibit functional Wnt signaling, both directly linked to IQGAP2-mediated tumor suppression. Their broad use in signal transduction and drug discovery provides a relevant context for studying IQGAP2 loss.
IQGAP2 scaffolds interactions among calmodulin, Cdc42, Rac1, actin, ??-catenin, E-cadherin, APC, and CLIP-170, connecting adhesion complexes to the cytoskeleton. It is transcriptionally activated by Wnt/??-catenin/TCF and feeds back to suppress ??-catenin activity by stabilizing adherens junctions. IQGAP2 loss relieves this inhibition, enhancing ??-catenin nuclear translocation and TCF/LEF target gene expression, while also potentiating MAPK/ERK and PI3K/Akt signaling. This disrupts cell polarity, increases proliferation, and promotes migration.
In HT29 cells, IQGAP2 knockout mirrors its frequent downregulation in colorectal tumors, weakening E-cadherin adhesion and driving EMT-like changes and enhanced invasion. The mucin-producing, differentiation-competent nature of HT29 further permits analysis of epithelial barrier integrity and differentiation. The polyclonal knockout population reflects tumor heterogeneity, making it suitable for unbiased studies of variable pathway responses and oncogenic signaling.
Typical assays include western blotting for ??-catenin and phospho-ERK1/2, RT-qPCR for TCF/LEF target genes, immunofluorescence for E-cadherin and actin, and co-immunoprecipitation of IQGAP2 with Cdc42 or calmodulin. Functional studies can employ scratch assays, Boyden chamber invasion, TEER measurements, and Wnt reporter assays (TOP/FOP flash). The model supports drug screening for Wnt or MAPK inhibitors and transcriptomic profiling by RNA-seq. For inquiries, contact Ascent Research.
