The CC2D1A Knockout AGS Polyclonal Cells are a CRISPR/Cas9-mediated loss-of-function model generated from the AGS human gastric adenocarcinoma cell line. This polyclonal population consists of a heterogeneous pool of cells carrying diverse gene-disrupting modifications at the CC2D1A locus, eliminating functional protein expression. The polyclonal format facilitates robust functional studies without clonal selection, capturing a broad spectrum of knockout events to assess the overall impact of CC2D1A deficiency in an epithelial context.
The AGS host cell line is an adherent epithelial model derived from a human gastric adenocarcinoma, widely employed in gastric cancer research. These cells retain key characteristics of gastric mucosal epithelium, including secretory capabilities and barrier functions, making them a physiologically relevant system to investigate tumor biology and signal transduction pathways underlying gastric carcinogenesis.
CC2D1A functions as a transcriptional repressor that modulates multiple signaling cascades. It directly binds the HTR1A serotonin receptor promoter and recruits HDAC1/2-containing corepressor complexes to silence transcription. In the NF-??B pathway, CC2D1A interacts with RELA (p65) and inhibits NF-??B-dependent gene expression, such as IL-8 and Bcl-2 family members. Additionally, CC2D1A associates with the Notch coactivator MAML1, antagonizing the transcription of Notch target genes including HES1 and HEY1. Upstream stimuli such as TNF-?? and pro-inflammatory cytokines regulate CC2D1A activity, positioning it as a convergence point between NF-??B, Notch, and serotonin receptor signaling.
Disruption of CC2D1A in AGS cells is particularly relevant for dissecting its tumor-suppressive or regulatory roles in gastric adenocarcinoma. Loss of CC2D1A is expected to derepress NF-??B and Notch transcriptional programs, potentially affecting cell proliferation, survival, apoptosis, and migration. Given the established link between chronic inflammation and gastric cancer, this knockout model provides a platform to investigate how CC2D1A-mediated inhibition of inflammatory signaling influences tumorigenic processes within a gastric mucosal epithelial background.
This CC2D1A knockout polyclonal model supports a wide range of experimental applications, including NF-??B and Notch luciferase reporter assays to quantify pathway activity, cytokine secretion ELISAs for measuring IL-8 release, ChIP-qPCR to examine HTR1A promoter occupancy, and co-immunoprecipitation studies to probe interactions with RELA or HDAC1. It is also suited for cell viability, apoptosis, and migration assays in the context of drug discovery targeting NF-??B and Notch pathways. For technical inquiries and ordering information, please contact Ascent Research.
