The CD109 Knockout AGS Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population targeting CD109 in the AGS human gastric adenocarcinoma epithelial cell line. This gene disruption model is generated using CRISPR/Cas9-mediated gene editing to introduce loss-of-function modifications across a heterogeneous cell pool, providing a versatile tool for studying CD109-dependent biology without clonal selection biases. The polyclonal format ensures that a broad spectrum of genetic alterations is represented, enabling robust analysis of population-level phenotypes.
AGS cells are a widely utilized model of gastric adenocarcinoma, originally derived from a primary tumor of a patient with stomach cancer. These epithelial cells retain key characteristics of gastric cancer, including active proliferation, migration, and invasion programs, and are commonly employed to investigate oncogenic signaling, tumor microenvironment interactions, and drug response mechanisms. Their genetic background and well-characterized signaling networks make them particularly suitable for dissecting the roles of cell surface receptors and co-receptors in cancer progression.
CD109 is a GPI-anchored glycoprotein and TGF-beta co-receptor that binds TGFBR1/TGFBR2 and promotes their clathrin-mediated endocytosis via interactions with CLTC and CAV1, leading to receptor degradation and attenuated SMAD2/3 phosphorylation. This negatively regulates TGF-beta transcriptional outputs, including SERPINE1 expression. CD109 also interacts with EGFR, modulating its trafficking and downstream ERK1/2 (MAPK3/MAPK1) signaling. Upstream regulators such as TGF-beta, EGF, SMAD3, and STAT3 control CD109 expression, placing it at the intersection of these pathways.
In AGS gastric cancer cells, CD109 is frequently overexpressed and promotes migration, invasion, and resistance to therapy. Disrupting CD109 in this polyclonal model allows investigation of its contributions to TGF-beta and EGFR signaling crosstalk, endocytic trafficking, and epithelial-mesenchymal transition. The model is valuable for assessing how CD109 loss alters responses to TGF-beta, EGF, and chemotherapeutics, yielding insights into gastric adenocarcinoma progression.
Research applications include western blotting for phospho-SMAD2/3, TGF-beta reporter assays, MTT proliferation, wound healing migration, transwell invasion, and immunofluorescence for EGFR localization. Co-immunoprecipitation validates CD109-TGFBR1 interactions, and qPCR quantifies TGF-beta targets such as SERPINE1 and COL1A1. This model supports studies on TGF-beta/EGFR crosstalk, tumor microenvironment, drug resistance, and therapeutic targeting in gastric and other cancers. For product inquiries and technical support, please contact Ascent Research.
