The CD276 Knockout HS-SY-2 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disrupted CD276 expression in the HS-SY-2 human synovial sarcoma line. This heterogeneous pool, generated via CRISPR/Cas9-mediated gene disruption, allows functional studies without single-clone isolation, preserving diversity. It is ideal for pooled assays, drug screens, and pathway analysis in immune checkpoint and tumor signaling research.
The parental HS-SY-2 line is a human synovial sarcoma model harboring the t(X;18) translocation and SS18-SSX fusion oncoprotein. These malignant mesenchymal cells display aggressive growth, migration, and invasion, making them a key tool for studying sarcoma biology and the interplay between oncogenic drivers and immune modulators like CD276.
CD276 (B7-H3) is a B7 family immune checkpoint molecule that also functions as a tumor-intrinsic signaling receptor. It interacts with the counter-receptor TLT-2 on T cells to suppress anti-tumor immunity. In tumor cells, CD276 signaling activates the PI3K/AKT and MAPK/ERK cascades, driving proliferation, survival, and motility. Key upstream regulators include STAT3, NF-??B, and IRF1, which respond to cytokines like IFN-?? and growth factors such as EGF. Downstream, CD276 upregulates MMP-2 and MMP-9, facilitating invasion, and increases cyclin D1 expression to promote cell cycle progression. This positions CD276 at the intersection of immune evasion and oncogenic signaling.
In synovial sarcoma, CD276 is often highly expressed, and its role in suppressing anti-tumor immune responses while promoting aggressive tumor cell behavior makes it a compelling therapeutic target. The CD276 knockout HS-SY-2 polyclonal cells provide a unique system to dissect CD276-dependent phenotypes in the context of SS18-SSX-driven malignancy. Loss of CD276 function allows researchers to evaluate alterations in cell proliferation, migration, and invasion that are directly attributable to CD276 signaling, as well as to assess the impact on T-cell interactions. This model is particularly valuable for understanding how CD276 collaborates with the fusion oncoprotein to shape the tumor??s immunophenotype and metastatic potential.
This knockout model supports diverse assays, including T cell cytotoxicity co-cultures for immune evasion studies, and screening of anti-CD276 antibodies or small molecules. Standard analyses??western blotting, RT-qPCR, flow cytometry??confirm CD276 loss and pathway alterations. Migration and invasion assays, along with phospho-AKT/ERK analysis, directly assess CD276-driven signaling. These applications enable mechanistic dissection of CD276 in sarcoma biology and preclinical therapeutic evaluation. For further details, please contact Ascent Research.
