The HMMR Knockout HT29 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from HT29 cells, featuring targeted disruption of the HMMR gene. This product provides a loss-of-function model for studying hyaluronan-mediated motility and receptor function in a colorectal adenocarcinoma background. The polyclonal nature of the knockout pool reflects a heterogeneous collection of gene-edited cells, enabling robust representation of diverse editing outcomes without clonal isolation.
The parental HT29 cell line originates from a primary colorectal adenocarcinoma isolated from a 44-year-old female donor and exhibits an adherent epithelial morphology. HT29 cells serve as a widely employed model for intestinal epithelial barrier function, colorectal adenocarcinoma biology, and anticancer drug testing. Their properties make them an appropriate host for investigating signaling pathways relevant to colorectal tumor progression.
HMMR (also known as RHAMM) encodes a receptor for hyaluronan that promotes cell motility and proliferation through activation of downstream effectors including FAK, ERK1/2, and Akt. It interacts directly with hyaluronan and CD44, and associates with the microtubule network via tubulin. Upstream regulators such as EGF, TGF-beta, and hyaluronan oligosaccharides stimulate HMMR expression, while its signaling converges on RhoA, Rac1, and the PI3K/Akt and MAPK/ERK pathways to drive cytoskeletal reorganization and migration.
In the HT29 context, HMMR contributes to the motile and invasive phenotype characteristic of colorectal adenocarcinoma progression. Disruption of HMMR in these cells allows dissection of its specific roles in hyaluronan-induced signaling, cell migration, and wound healing, providing a physiologically relevant system to evaluate the contribution of this receptor to tumor cell behavior. The knockout model is particularly suited to differentiate HMMR-dependent from HMMR-independent mechanisms in colorectal cancer cell motility.
Typical applications include wound healing assays and transwell migration or invasion assays to assess cell motility and invasiveness, western blotting to measure ERK1/2 and Akt phosphorylation, immunofluorescence staining for hyaluronan distribution, proliferation assays, RNA-seq transcriptomic profiling, and co-immunoprecipitation with CD44 to probe receptor-hyaluronan interactions. These cells also support drug screening efforts aimed at identifying HMMR-targeted therapeutics. For additional technical details, please contact Ascent Research.
