The EBAG9 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line. This product features targeted disruption of the EBAG9 gene, generating a loss-of-function model for studying immune evasion, apoptosis regulation, and estrogen receptor signaling. As a polyclonal population, these cells are ideal for functional assays requiring allelic diversity within a consistent genetic background.
The HT29 cell line is an epithelial-like model originally derived from a primary colon adenocarcinoma of a 44-year-old female. It is widely employed in colorectal cancer research and drug discovery due to its tumorigenic properties and epithelial characteristics. HT29 cells retain key features of colorectal adenocarcinoma, making them relevant for investigating oncogenic pathways. The polyclonal knockout format maintains this genetic background while introducing a targeted loss of EBAG9 function.
EBAG9 encodes a protein that promotes immune evasion by regulating apoptosis and immune checkpoint signaling. Its transcription is activated by estrogen and IFN-??, linking hormone signaling to immune suppression. The protein interacts with estrogen receptor alpha and immune checkpoint receptors, and its downstream effects include T cell apoptosis and immune suppression. Mechanistically, EBAG9 functions as a negative regulator of immune surveillance. Knockout of EBAG9 is expected to impair these evasion mechanisms, sensitizing tumor cells to immune-mediated killing and apoptosis.
In HT29 colorectal adenocarcinoma cells, ablation of EBAG9 dissects the intersection of estrogen receptor signaling and immune evasion. Colorectal tumors exploit immune checkpoints to evade immunity, and EBAG9 loss provides a model to study tumor?Cimmune interactions. The knockout is anticipated to enhance vulnerability to immune effector cells and pro-apoptotic stimuli, offering a platform to test immunotherapies. The HT29 background also allows assessment of estrogen-related signaling crosstalk in a colon-derived context.
These polyclonal EBAG9 knockout cells are suitable for studying tumor immune evasion, apoptosis signaling, and drug sensitivity in colorectal cancer. Assays include western blotting, RT-qPCR, flow cytometry for immune markers and apoptosis, co-culture with immune cells, and migration/invasion assays. The loss-of-function model facilitates investigations into EBAG9’s role in oncogenesis and immune modulation. For more information or to request a quote, please contact Ascent Research.
