In Stock Cell Lines
The Adgre5 Knockout MC38 Cell Line is a CRISPR/Cas9-edited knockout cell line targeting the Adgre5 gene in the MC38 murine colon adenocarcinoma cell line. Adgre5 encodes the adhesion G protein-coupled receptor CD97, which mediates cell adhesion, migration, and immune modulation through interactions with CD55, integrins, and downstream activation of RhoA and ERK signaling. This knockout model enables detailed investigation of CD97's role in colorectal cancer progression, tumor metastasis, and immune cell cross-talk. Typical applications include transwell migration assays, cell adhesion studies, syngeneic xenograft tumor models, and co-culture experiments with immune cells. For more information, contact Ascent Research.
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The Adgre5 Knockout MC38 Cell Line is a CRISPR/Cas9-edited knockout cell line that disrupts the Adgre5 gene in the MC38 murine colon adenocarcinoma background. This gene-edited product provides a clean loss-of-function system for studying the adhesion G protein-coupled receptor CD97, encoded by Adgre5. By ablating CD97 expression, the cell line eliminates its downstream signaling cascades and adhesion functions, making it a powerful tool for dissecting tumor biology and immune interactions in a syngeneic colorectal cancer model.
The MC38 cell line is a murine colon adenocarcinoma derived from C57BL/6 mice, extensively employed as a syngeneic model for colorectal cancer and tumor immunology research. Its immunogenic nature permits robust investigation of host immune responses when implanted into immunocompetent C57BL/6 recipients, making it particularly suitable for evaluating tumor?Cimmune cell cross-talk and immunotherapeutic interventions. The Adgre5 knockout in this context enables specific interrogation of CD97-dependent mechanisms within the colorectal cancer microenvironment.
Adgre5 encodes CD97, an adhesion G protein-coupled receptor that mediates cell adhesion, migration, and immune modulation. CD97 interacts with the cell surface ligand CD55 (decay-accelerating factor), chondroitin sulfate, and integrin ??1, coupling to G??12/13 and G??q/11 to activate downstream effectors. Canonical signaling downstream of CD97 includes activation of the small GTPase RhoA and its effector ROCK, as well as the ERK1/2 MAP kinase pathway, ultimately modulating transcription factors such as NF-??B. These pathways regulate cytoskeletal dynamics, matrix adhesion, and inflammatory gene expression. Disruption of Adgre5 abolishes CD97-mediated adhesion and signaling, impairing tumor cell migration and reducing cross-talk with CD55-expressing stromal or immune cells.
In the MC38 colorectal cancer model, CD97 contributes to tumor cell invasion, metastatic dissemination, and modulation of the immune microenvironment. CD55 expressed on fibroblasts, endothelial cells, and immune cells can engage CD97 on tumor cells, triggering pro-migratory and survival signals. By eliminating this receptor?Cligand interaction, the Adgre5 Knockout MC38 Cell Line serves as a critical tool to dissect the role of CD97 in tumor?Cstromal communication, immune evasion, and the transition to metastatic disease. This model is also valuable for exploring connections to inflammatory bowel disease, where CD97 has been implicated in intestinal inflammation and tissue remodeling.
Researchers can employ this knockout cell line in a variety of functional assays to probe CD97-related biology. Flow cytometry and Western blotting confirm loss of Adgre5/CD97 expression. Transwell migration and cell adhesion assays quantify the impact on motility and substrate attachment. In vivo, syngeneic xenograft tumor growth studies with C57BL/6 mice reveal consequences on tumor progression and metastasis. Co-culture systems with macrophages or other immune cells assess how CD97 loss alters tumor?Cimmune cell cross-talk and cytokine profiles. For detailed technical information or ordering inquiries, please contact Ascent Research.
