Description

The CD70 Knockout BT-549 Cell Line is a human CRISPR/Cas9-engineered breast carcinoma epithelial cell model in which the CD70 gene has been disrupted to eliminate functional CD70 expression. This edited line provides a stable in vitro system for investigating the consequences of CD70 loss in a triple-negative breast cancer-relevant background. As a defined knockout model derived from BT-549 cells, it is suited for mechanistic studies requiring controlled comparison of CD70-dependent and CD70-independent cellular phenotypes, signaling outputs, and immune interaction profiles.

BT-549 is a human breast ductal carcinoma cell line widely used as a model of triple-negative breast cancer with mesenchymal-like features. It is experimentally valuable for studying tumor progression-related behaviors, including proliferation, migration, invasion, and cytokine-responsive signaling. Because BT-549 cells are commonly applied in analyses of tumor cell plasticity, inflammatory pathway regulation, and therapeutic response, they provide a relevant host background for examining how loss of an immune modulatory surface ligand alters cancer-associated signaling states and tumor cell interactions with the microenvironment.

CD70 encodes a type II transmembrane ligand of the TNF superfamily that binds the receptor CD27 and mediates costimulatory signaling in immune cells. CD70 is regulated by inflammatory and stress-associated inputs including NF-kB, IFNG, TNF, IL1B, and T-cell receptor-associated inflammatory signaling. Upon CD27 engagement, CD70-dependent signaling promotes recruitment of TRAF2 and TRAF5 and contributes to downstream activation of canonical and noncanonical NF-kB pathway components, including NFKB1/RELA and RELB/NFKB2. These events are associated with induction of targets such as NFKBIA, as well as enhanced T-cell proliferation, cytokine production, and survival signaling in activated lymphocytes. In cancer, this ligand-receptor axis is relevant to tumor-immune crosstalk, immune evasion, and inflammatory signaling networks.

In the BT-549 context, CD70 knockout enables direct investigation of how a tumor-associated immune ligand contributes to breast cancer cell behavior and communication with CD27-positive immune cells. This model is useful for dissecting whether cytokine-induced inflammatory states, NF-kB-associated transcriptional programs, or tumor cell phenotypes linked to migration and invasion are altered when CD70 is absent. It also supports comparative studies of pathway dependency and gene-regulatory changes in a triple-negative breast cancer background.

Applications include flow cytometry, western blotting, and RT-qPCR to confirm loss of CD70-associated expression; RNA-seq to profile transcriptional consequences of knockout under basal or IFNG, TNF, or IL1B stimulation; and NF-kB reporter assays to assess effects on inflammatory signaling outputs. In co-culture systems with CD27-positive immune cells, the model can be used to evaluate effects on lymphocyte activation, cytokine production, or apoptosis-related responses. Additional use cases include co-immunoprecipitation or immunofluorescence for pathway interrogation, cytokine profiling, proliferation assays, migration and invasion studies, and drug sensitivity testing in immuno-oncology or combination-treatment workflows. Researchers may contact Ascent Research for additional technical information, product details, or related gene-edited cell models.