The DPYSL2 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from HT29 human colorectal adenocarcinoma epithelial cells, designed for loss-of-function studies of DPYSL2 (collapsin response mediator protein 2, CRMP2). This product employs CRISPR/Cas9-mediated gene disruption, yielding a heterogeneous mixture of edited cells suitable for functional genomics and cancer research applications.
HT29 is a well-established human colorectal adenocarcinoma cell line isolated from a primary tumor of a female Caucasian. It exhibits epithelial morphology and can be differentiated into enterocyte-like cells, serving as a model for intestinal differentiation, barrier function, and colorectal cancer progression. HT29 is frequently utilized in metastasis and cell migration studies.
DPYSL2 encodes a microtubule-associated phosphoprotein that mediates semaphorin 3A/plexin-A signaling to regulate cytoskeletal dynamics. It functions downstream of semaphorin 3A, neuropilin-1, and plexin-A, and its activity is modulated by phosphorylation via upstream kinases GSK3??, Cdk5, and ROCK. CRMP2 binds directly to tubulin, endophilin, neurofibromin, and other CRMP family members, integrating extracellular guidance cues with microtubule polymerization and actin remodeling. In this capacity, DPYSL2 is crucial for cell migration, neurite outgrowth, and cytoskeletal maintenance. Its disruption in HT29 cells therefore disables a central node of the semaphorin signaling-cytoskeletal axis.
Given HT29’s relevance in colorectal cancer metastasis, the DPYSL2 knockout polyclonal cells offer a unique platform to examine the non-neuronal functions of CRMP2 in tumor cell motility. Loss of CRMP2 impairs microtubule stability and migratory capacity, simulating aspects of cancer cell dissemination. As a polyclonal population, this model reflects varied editing events, providing a practical system for high-throughput or bulk experimental readouts without the need for clonal expansion.
Researchers can employ this knockout model in scratch wound healing and Boyden chamber invasion assays, western blotting and RT-qPCR validation, immunofluorescence for microtubule organization, and phospho-specific immunoblotting to assess GSK3?? and Cdk5 activity. It supports colorectal cancer metastasis research, cytoskeletal dynamics studies, semaphorin signaling investigations, and preclinical validation of therapeutic targets. For additional information or custom requests, contact Ascent Research.
