The Hyal2 Knockout GL261 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the mouse glioma cell line GL261, engineered for loss-of-function studies of the Hyal2 gene. This product provides a heterogeneous pool of edited cells with targeted disruption of Hyal2, offering a robust model for functional genomics and cancer biology research without requiring single-cell clonal isolation.
The GL261 cell line, established from a C57BL/6 mouse, is a widely used syngeneic model of glioblastoma multiforme, characterized by highly invasive and proliferative behavior in vitro and in vivo. Its immunocompetent background enables studies within the tumor microenvironment, making it particularly valuable for evaluating tumor-host interactions and therapeutic responses in brain cancer.
Hyal2 encodes hyaluronidase 2, a GPI-anchored enzyme that cleaves high-molecular-weight hyaluronan into low-molecular-weight fragments. These fragments serve as ligands for receptors CD44 and RHAMM, activating downstream signaling cascades including ERK, AKT, and NF-??B pathways. Hyal2 expression is regulated by upstream factors such as EGF, TGF-??, IL-1??, TNF-??, and HIF-1??, and its activity modulates matrix metalloproteinases (MMP-2, MMP-9) and cytoskeletal dynamics through Rac. This network promotes glioma cell migration, invasion, and angiogenesis, positioning Hyal2 at a critical nexus of hyaluronan metabolism and oncogenic signaling.
In the GL261 glioblastoma context, disruption of Hyal2 is expected to alter hyaluronan catabolism, potentially reducing generation of pro-inflammatory and pro-migratory hyaluronan fragments. This knockout model enables dissection of Hyal2-dependent contributions to CD44 and RHAMM activation, ERK/AKT/NF-??B signaling, and MMP-mediated extracellular matrix remodeling. Consequently, it provides a valuable tool for investigating mechanisms of glioma invasion and the role of hyaluronan in tumor progression and angiogenesis.
Researchers can employ this polyclonal knockout population in a variety of experimental settings, including tumor invasion and migration assays, hyaluronan ELISA quantification, Western blotting and RT-qPCR validation of gene disruption, CD44 and RHAMM flow cytometry, and immunofluorescence for HA binding. Additional applications encompass drug response screening, tumor microenvironment modeling, and nanoparticle uptake studies. Transcriptional profiling via RNA-seq further supports systems-level analyses of Hyal2-dependent gene networks. For further information, please contact Ascent Research.
