The CD47 Knockout HGC-27 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout population of HGC-27 gastric adenocarcinoma epithelial cells, in which the CD47 gene has been disrupted to eliminate expression of the target protein. This polyclonal knockout pool provides a heterogeneous loss-of-function model, suitable for experiments where gene disruption at the population level is sufficient for functional studies without clonal isolation. The product enables investigation of CD47-mediated signaling and its role in immune evasion and tumor progression, offering a versatile tool for cancer biology research.
The HGC-27 host cell line was originally derived from a metastatic lymph node of a gastric cancer patient, establishing it as a clinically relevant model of gastric adenocarcinoma with high metastatic potential. These epithelial cells retain key characteristics of invasive gastric carcinoma, including the capacity for migration and adhesion, making them particularly valuable for studying the molecular mechanisms underlying metastasis. The HGC-27 background provides a physiologically relevant context for assessing the functional consequences of CD47 disruption in a setting that recapitulates advanced-stage disease.
CD47 is a cell-surface glycoprotein that functions as an immune checkpoint by engaging the inhibitory receptor SIRP?? on macrophages, triggering the recruitment and activation of SHP-1 and SHP-2 phosphatases. This signaling cascade suppresses phagocytosis, effectively transmitting a “don’t eat me” signal that allows cancer cells to evade innate immune clearance. In addition to its immunomodulatory role, CD47 participates in integrin signaling and cytoskeletal remodeling through interactions with thrombospondin-1, integrin ??v??3, and VEGFR2. Upstream regulators such as HIF-1??, NF-??B, and the MYC oncogene drive CD47 expression in response to inflammatory cytokines and hypoxic tumor microenvironments. Downstream, CD47-mediated signaling converges on effectors including FAK and Rho GTPases to coordinate cell migration and adhesion. Disruption of CD47 abrogates SIRP?? engagement, releasing the phagocytic brake and restoring macrophage-mediated tumor cell clearance.
In the HGC-27 gastric cancer model, loss of CD47 expression is particularly significant given the prominent role of immune evasion in gastric carcinoma progression and metastasis. By eliminating the key suppressor of macrophage phagocytosis, these polyclonal knockout cells create a system to dissect how CD47 blockade re-activates innate immunity against metastatic tumor cells. This model simultaneously allows researchers to examine the impact of CD47 deficiency on integrin-dependent adhesive and migratory properties that are critical for metastatic dissemination, providing a multifaceted view of CD47’s contributions to gastric cancer aggressiveness.
These CD47 Knockout polyclonal cells are well-suited for a range of advanced research applications, including immune checkpoint blockade studies using macrophage phagocytosis rescue assays, where restoration of tumor cell clearance can be quantitatively measured. Flow cytometry can be employed to verify loss of CD47 surface expression, while western blotting enables analysis of downstream SHP-1/SHP-2 and FAK signaling changes. The cells are applicable in transwell migration and invasion assays to probe CD47-dependent motility, and in xenograft models for in vivo monitoring of tumor growth and metastasis. Additionally, they serve as a platform for screening combination therapies that pair phagocytosis enhancement with other modalities. For additional information, please contact Ascent Research.
