The PEG10 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric adenocarcinoma epithelial cell line AGS, designed for loss-of-function studies of the PEG10 gene. These cells harbor a pool of gene disruptions introduced by CRISPR/Cas9, providing a versatile model without clonal selection. The polyclonal nature captures diverse editing outcomes, making it suitable for investigating the functional impact of PEG10 inactivation in a gastric cancer context.
The AGS cell line is a well-established model of gastric adenocarcinoma, characterized by adherent epithelial morphology and oncogenic properties such as high proliferation and apoptosis resistance. It is extensively used to study signaling pathways underlying gastric tumorigenesis and to evaluate therapeutic interventions, offering a clinically relevant background for analyzing PEG10-driven mechanisms.
PEG10 encodes a paternally expressed retrotransposon-derived protein that promotes cell proliferation and inhibits apoptosis through modulation of TGF-beta, Wnt, and PI3K/AKT pathways. It directly interacts with the E3 ubiquitin ligase SIAH1, influencing the stability of downstream targets including BCL2 family members and TGF-beta signaling effectors. Upstream regulators include c-Myc, SP1, and imprinting control region methylation, while downstream mediators such as SMAD2, SMAD3, and BAX transduce its oncogenic signals. In gastric cancer, PEG10 overexpression disrupts TGF-beta-mediated tumor suppression by promoting degradation of TGFBR1 via SIAH1, enhancing cell survival.
In the AGS background, knockout of PEG10 attenuates the malignant phenotype, reducing proliferation, increasing apoptosis, and impairing migration. This polyclonal knockout model enables robust comparative analyses with wild-type AGS cells, facilitating the dissection of PEG10’s role in gastric adenocarcinoma and its interplay with critical signaling networks. It is especially valuable for studying imprinted retrotransposon-derived oncogenes and for validating PEG10 as a therapeutic target.
Typical applications include functional studies of imprinted genes in cancer, investigation of retrotransposon-derived protein mechanisms, and screening of small-molecule inhibitors targeting PEG10. The cells are compatible with proliferation assays (MTT/CCK-8), apoptosis detection (Annexin V), Western blotting, RT-qPCR, co-immunoprecipitation for PEG10-SIAH1 interaction, Transwell migration/invasion assays, and xenograft tumor growth studies. For further details, contact Ascent Research.
